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An integrative assessment of brain and body function 'at rest' in panic disorder: A combined quantitative EEG/autonomic function study
Abstract
We conducted a quantitative electroencephalographic (QEEG) and autonomic assessment of panic disorder (PD). The study samples comprised 52 individuals meeting DSM-IV criteria for PD (with or without agoraphobia) and 104 age-, gender-, and handedness-matched controls. EEG data were acquired from 16 scalp sites during resting eyes-open (REO) and eyes-closed (REC) conditions, and spectral power was assessed within 4 frequency bands: theta, alpha-1, alpha-2, and beta. The main findings were an overall reduction of spectral power in PD, compared to controls (Group main effect, p=.011), which was most apparent during REC (Group Condition interaction, p=.014), and within the alpha-1 frequency band (8-11 Hz; Group Band interaction, p=.014). Alpha-1 desynchronization occurs in response to increases in non-specific information processing, and aspects of attention such as alertness. Other findings were region-specific alterations of spectral power at frontal and temporal scalp sites, including a frontal alpha-1 asymmetry (R<L power) during REC in patients, but not controls. Findings for concomitantly-recorded autonomic measures included elevated heart rate, lower heart rate variability, and reduced rate of decrement of skin conductance level in patients, compared to controls. Finally, analyses examining the within-subjects relationship of central and peripheral function measures showed a differential pattern in patients and controls. Possible causes of these disturbances of brain and body function 'at rest', such as patients' ongoing automatic and strategic engagement with multiple disorder-related threat cues, including somatic variability and the testing environment, are discussed.
... Additional findings showed lower parietal alpha in response to panic-related vs. neutral pictures in individuals with PD, but not in controls. More recently, resting state EEG alpha asymmetry and alpha power were studied in 52 males and females with PD and comorbid disorders, including OCD, PTSD, GAD, and MDD, compared to 104 healthy controls (Wise et al., 2011). Alpha activity was analyzed in the alpha 1 (8-11 Hz) and alpha 2 (11-13 Hz) frequency ranges. ...
... Consisted with the observation that GAD is underresearched (Dugas et al., 2010;MacNamara and Proudfit, 2014), we found only one study assessing alpha abnormalities in this disorder (Saletu-Zyhlarz et al., 1997). With regards to alpha power alterations, anxious individuals (GAD patients and nonclinical individuals) show enhanced alpha power (Knyazev et al., 2004(Knyazev et al., , 2003(Knyazev et al., , 2002Saletu-Zyhlarz et al., 1997); no alterations were found in social phobia (Sachs et al., 2004); and decreased alpha (Newman et al., 1992;Wise et al., 2011) or no power alterations (Knott et al., 1997) were found in panic disorder. Examination of alpha asymmetry patterns generally revealed higher left relative to right frontal alpha activity (Crost et al., 2008;Davidson et al., 2000;Mathersul et al., 2008;Wiedemann et al., 1999;Wise et al., 2011), suggesting enhanced right frontal activity. ...
... With regards to alpha power alterations, anxious individuals (GAD patients and nonclinical individuals) show enhanced alpha power (Knyazev et al., 2004(Knyazev et al., , 2003(Knyazev et al., , 2002Saletu-Zyhlarz et al., 1997); no alterations were found in social phobia (Sachs et al., 2004); and decreased alpha (Newman et al., 1992;Wise et al., 2011) or no power alterations (Knott et al., 1997) were found in panic disorder. Examination of alpha asymmetry patterns generally revealed higher left relative to right frontal alpha activity (Crost et al., 2008;Davidson et al., 2000;Mathersul et al., 2008;Wiedemann et al., 1999;Wise et al., 2011), suggesting enhanced right frontal activity. However, in some cases this pattern differed by anxiety (Mathersul et al., 2008) or PD (Locatelli et al., 1993) subtype and was sensitive to the context in which asymmetry was measured (Crost et al., 2008;Davidson et al., 2000;Wiedemann et al., 1999), and in others, no alpha asymmetry was found (Beaton et al., 2008). ...
... This analysis predicts subsequent cognitive and perceptual ability in a frequency-specific domain. 11 Absolute power is defined as the total energy in an electrode located at a cortical area in a specific frequency. 12 Relative power represents the percentage of power in any band compared with the total power in EEG. ...
... Wise et al. 11 conducted a quantitative electroencephalographic (qEEG) and autonomic assessment of 52 PD patients, with or without agoraphobia. EEG data ...
... 20 The major findings on alpha and beta rhythms in anxiety point to a lower intensity of the alpha rhythm while high-frequency beta rhythms are greater. 11,20,28,[35][36][37][38] Although these are not the only findings, they are the most reliable among the different studies and they are also consistent with the hypothesis of the fear neurocircuitry. ...
Some studies have reported the importance of electroencephalography (EEG) as a method for investigating abnormal parameters in psychiatric disorders. Different findings in time and frequency domain analysis with regard to central nervous system arousal during acute panic states have already been obtained. This study aimed to systematically review the EEG findings in panic disorder (PD), discuss them having a currently accepted neuroanatomical hypothesis for this pathology as a basis, and identify limitations in the selected studies. Literature search was conducted in the databases PubMed and ISI Web of Knowledge, using the keywords electroencephalography and panic disorder; 16 articles were selected. Despite the inconsistency of EEG findings in PD, the major conclusions about the absolute power of alpha and beta bands point to a decreased alpha power, while beta power tends to increase. Different asymmetry patterns were found between studies. Coherence studies pointed to a lower degree of inter-hemispheric functional connectivity at the frontal region and intra-hemispheric at the bilateral temporal region. Studies on possible related events showed changes in memory processing in PD patients when exposed to aversive stimuli. It was noticed that most findings reflect the current neurobiological hypothesis of PD, where inhibitory deficits of the prefrontal cortex related to the modulation of amygdala activity, and the subsequent activation of subcortical regions, may be responsible to trigger anxiety responses. We approached some important issues that need to be considered in further researches, especially the use of different methods for analyzing EEG signals. Keywords: Electroencephalography, panic disorder, neurobiology, brain mapping.
... Previous studies revealed that notable dysfunction has been observed in both the frontal region of the brain and the hypothalamicpituitary-adrenal (HPA) axis in patients with PD [17]. Despite the scarcity of resting-state EEG studies, a consistent pattern among PD patients has been observed, characterized by decreased alpha band activity in the frontal and parietal regions and increased beta band activity in the frontal region [18][19][20][21]. The HPA axis is a neuroendocrine system that regulates the body's stress response, and it may disrupt the balance between excitatory and inhibitory neural activity, leading to changes in cortical activity [18,22]. ...
... Selected artifact-free EEG segments were used to calculate the eLORETA intracranial spectral density from 1 to 50 Hz with a resolution of 1 Hz. Functional eLORETA images of spectral density were computed for five frequency bands: delta (1-4 Hz), theta (4.5-8 Hz), alpha (8.5-12 Hz), beta (13)(14)(15)(16)(17)(18)(19)(20)(21)(22)(23)(24)(25)(26)(27)(28)(29)(30), and gamma . ...
Background: Obsessive–compulsive disorder (OCD) and panic disorder (PD) are debilitating psychiatric conditions, yet their underlying neurobiological differences remain underexplored. This study aimed to directly compare resting-state EEGs in patients with OCD and PD, without a healthy control group, using the eLORETA method. Methods: We collected retrospective EEG data from 24 OCD patients and 22 PD patients who were hospitalized due to significant impairment in daily life functions. eLORETA was used to analyze the EEG data. Results: Heightened theta activity was observed in the anterior cingulate cortex (ACC) of OCD patients compared to PD patients (PD vs. OCD, t = −2.168, p < 0.05). Conversely, higher gamma activity was found in the medial frontal gyrus (MFG) and paracentral lobule (PCL) in PD patients (PD vs. OCD, t = 2.173, p < 0.05). Conclusions: Our findings highlight neurobiological differences between OCD and PD patients. Specifically, the increased theta activity in the ACC for OCD patients and elevated gamma activity in the MFG and PCL for PD patients offer preliminary insights into the neural mechanisms of these disorders. Further studies are essential to validate these results and delve deeper into the neural underpinnings.
... As the EEG has been used for the functional network analysis in the topological changes associated with cognitive regions in real-time [18,[28][29][30], we aimed to observe the computer simulation effects on EEG alpha power and the reaction time for visual stimuli in the PD patients. Our electrophysiological variable of interest is the alpha absolute power due relationship with the top down and inhibitory processes [31][32][33][34]. This trait deficit in alpha activity has been proposed as a risk factor for several psychiatric disorders, including anxiety disorders [35]. ...
... Our main result indicated a decreased alpha power in PD patients, however demonstrated an increase in EEG alpha power after the computer simulation in both groups, except for the Fp1 electrode during M3 moment in the experimental group. According to previous studies, this result reported a low EEG alpha power in PD patients [9,[32][33][34]48,49]. Previous studies demonstrated a greater EEG alpha power for healthy subjects was found when compared to the PD patients in the frontal area. ...
Aim: The present study investigated the differences between the Panic Disorder (PD)
patients groups’ and healthy controls for the EEG alpha dynamics under the frontal cortex and
reaction time during the oddball task. Material and Methods: The reaction time during the oddball
paradigm concomitant to EEG alpha power was tested in nine PD patients and ten healthy controls
before and after a computer simulation presentation. Results: The findings revealed a decrease in
EEG alpha power in PD patients concerning the control group (p ≤ 0.0125). However, both groups
demonstrated an increased cortical oscillation after the computer simulation, except for the Fp1
electrode during M3 moment in the experimental group. The experimental group has a fast reaction
time compared to healthy individuals during the oddball task (p = 0.002). Conclusions: We propose
that the decrease in EEG alpha power in the PD patients may indicate an increase in processing
related to an anxiogenic stimulus and interference of the anxiety state that compromises the inhibitory
control. The reaction time task reveals cognitive symptoms in the experimental group, which may be
related to the faster reactivity and high impulsivity to stimuli.
... Different types of anxiety disorders demonstrated alpha abnormalities during both rest and provocation of anxiety [45]. Assessing alpha abnormalities in anxious individuals show enhanced alpha power in general anxiety [190][191][192][193], no alterations in social phobia [194] and decreased alpha [195,196] or no power alterations in panic disorder [197]. Behavioral inhibition and trait anxiety have shown a positive association with relative alpha power and a negative association with relative delta power in both females and males [190,191]. ...
... In addition, it has been shown that behavioral inhibition (BI) and trait anxiety are correlated with increased anticorrelation between alpha and delta bands [191,192]. Several studies investigating the alpha asymmetry patterns found enhanced left relative to right frontal alpha activity in generalized anxiety disorder (GAD) [142,198], in social phobia [199] in PD patients [196,200] and no group differences in alpha asymmetry during rest in individuals with high and low social anxiety [201]. ...
Background
A large body of evidence suggested that disruption of neural rhythms and synchronization of brain oscillations are correlated with variety of cognitive and perceptual processes. Cognitive deficits are common features of psychiatric disorders that complicate treatment of the motivational, affective and emotional symptoms.
Objective
Electrophysiological correlates of cognitive functions will contribute to understanding of neural circuits controlling cognition, the causes of their perturbation in psychiatric disorders and developing novel targets for treatment of cognitive impairments.
Methods
This review includes description of brain oscillations in Alzheimer’s disease, bipolar disorder, attentiondeficit/hyperactivity disorder, major depression, obsessive compulsive disorders, anxiety disorders, schizophrenia and autism.
Results
The review clearly shows that the reviewed neuropsychiatric diseases are associated with fundamental changes in both spectral power and coherence of EEG oscillations.
Conclusion
In this article we examined nature of brain oscillations, association of brain rhythms with cognitive functions and relationship between EEG oscillations and neuropsychiatric diseases. Accordingly, EEG oscillations can most likely be used as biomarkers in psychiatric disorders.
... All rights reserved. and that there is a decrease in theta, alpha-1, alpha-2, and beta power [65]. ...
... For dermatologists, the general view is that skin diseases such as psoriasis and eczema create susceptibility to psychiatric disorders by causing stigmatization, social isolation, and thus the impaired quality of life because of being visible [36,58,17]. On the other hand, there is an opinion that psychiatric disorders can be included in the etiology of skin diseases [65,32]. ...
Objective
Anxiety is commonly observed together with skin diseases and can aggravate them, while skin diseases can increase anxiety. The relationship of skin diseases observed in panic disorder with quantitative electroencephalography (QEEG) findings has not been investigated yet. The aim of this study is to compare the absolute alpha and delta power of panic disorder patients with and without skin disease.
Methods
246 panic disorder patients, 19 of whom had skin disease and 227 of whom did not have skin disease, were included in the study. Panic disorder severity scale (PDSS) scores of patients were recorded, and QEEG recording was performed. Absolute alpha and delta power and PDSS scores were compared between the two groups.
Results
It was found that the absolute delta power in the left hemisphere was lower and PDSS scores were higher in the patients with skin diseases compared to the control group. In the patients with skin disease, decreased delta power in the left hemisphere may cause impairment in the processing of positive emotions and may cause trait anxiety.
Conclusion
Trait anxiety may increase susceptibility to skin diseases by disrupting cutaneous homeostasis resulting from the prolonged sympathetic nervous system activation.
... Respiration is affected (speci cally hyperventilation) in anxiety disorders, as evidenced by decreased end-tidal CO 2 (ETCO 2 ) [8]. Finally, anxiety-related arousal can be detected centrally using electroencephalography (EEG), with some evidence that attenuated alpha activity is associated with anxiety [9]. Given the close association between physiological arousal and anxiety disorders, over the past several decades, there has been signi cant interest in the use of biofeedback, based on the notion that autonomic nervous system responses can be instrumentally conditioned [10]. ...
... Alpha is the dominant EEG rhythm in healthy adults at rest and is associated with a calm, relaxed state [28]. Among patients with panic disorder, alpha is attenuated [9], though in GAD patients, alpha is increased [29]. Increasing alpha magnitude can produce a calming effect in high-anxious individuals [30]. ...
Biofeedback refers to the operant training of physiological responding. Variants include electromyography (EMG), electrodermal activity (EDA), skin temperature, heart rate (HR) and heart rate variability (HRV), respiratory biofeedback of end-tidal CO2 (ETCO2), electroencephalography (EEG) signal, and blood oxygen-level dependent signal using functional magnetic resonance imaging (fMRI). This chapter presents a qualitative and quantitative systematic review of randomized controlled trials of biofeedback for anxiety disorders as defined by the 3rd through 5th editions of the Diagnostic and Statistical Manual of Mental Disorders (DSM). Meta-analytic results indicated that biofeedback (broadly defined) is superior to wait list, but has not been shown to be superior to active treatment conditions or to conditions in which patients are trained to change their physiological responding in a countertherapeutic direction. Thus, although biofeedback appears generally efficacious for anxiety disorders, the specific effects of biofeedback cannot be distinguished from nonspecific effects of treatment. Further, significant limitations were identified in the existing literature, with the majority receiving a “weak” rating according to Effective Public Health Practice Project (EPHPP) rating system guidelines. Future directions for research are discussed.
... Although there is not a consensus for the use of HRV in research on autonomic function disorder in mental disorders, HRV continues to be investigated as a candidate biomarker for a variety of mental disorders including anxiety disorders led by PD (Kotianova et al. 2018, Perini andVeicsteinas 2003), posttraumatic stress disorder (PTSD) and depression (Boettger and Hoyer 2006, Ito et al. 1999, Nahshoni et al. 2004, Udupa et al. 2007, Peschel et al. 2016, Friedman 2007, Shinba 2017). Research has demonstrated increased heart rate in patients with PD diagnosis at rest compared to healthy controls (Martinez et al. 2010, Friedman and Thayer 1998, Cohen et al. 2009, Garakini et al. 2009, Wise et al. 2011), reduction in HRV (McCraty et al. 2001, Hovland et al. 2012, Martinez et al. 2010, Wise et al. 2011, Yeragani et al. 2003, Diveky 2012, reduced vagal tonus and a relative increase in sympathetic system efficacy (McCraty et al. 2001, Yeragani et al. 1993, Klein et al. 1995, Friedman and Thayer 1998, Chalmers and Quintana 2014, Cohen and Benjamin 2006. Furthermore, an association was reported between the anxiety level and the reduction in frequency dependent parameters, such as HF, that reflect parasympathetic activity in HRV (Miu et al. 2009). ...
... Although there is not a consensus for the use of HRV in research on autonomic function disorder in mental disorders, HRV continues to be investigated as a candidate biomarker for a variety of mental disorders including anxiety disorders led by PD (Kotianova et al. 2018, Perini andVeicsteinas 2003), posttraumatic stress disorder (PTSD) and depression (Boettger and Hoyer 2006, Ito et al. 1999, Nahshoni et al. 2004, Udupa et al. 2007, Peschel et al. 2016, Friedman 2007, Shinba 2017). Research has demonstrated increased heart rate in patients with PD diagnosis at rest compared to healthy controls (Martinez et al. 2010, Friedman and Thayer 1998, Cohen et al. 2009, Garakini et al. 2009, Wise et al. 2011), reduction in HRV (McCraty et al. 2001, Hovland et al. 2012, Martinez et al. 2010, Wise et al. 2011, Yeragani et al. 2003, Diveky 2012, reduced vagal tonus and a relative increase in sympathetic system efficacy (McCraty et al. 2001, Yeragani et al. 1993, Klein et al. 1995, Friedman and Thayer 1998, Chalmers and Quintana 2014, Cohen and Benjamin 2006. Furthermore, an association was reported between the anxiety level and the reduction in frequency dependent parameters, such as HF, that reflect parasympathetic activity in HRV (Miu et al. 2009). ...
Objective: One of the methods used to assess autonomic nervous system dysfunction in the etiology of panic disorder (PD) is heart rate variability (HRV). HRV is controlled by the sympathetic and parasympathetic (vagal) branches of the autonomic nervous system and reflects the capacity of autonomic stimulation by the parasympathetic system. The aim of this study was to evaluate heart rate variability (HRV) time domain parameters based on twenty four hour holter ECG analysis among drug-naive patients with panic disorder (PD) without any other medical and psychiatric comorbidity. Method: The study group consisted of 41 patients with PD and 46 healthy controls. Participants were evaluated with SCID-1 for psychiatric diagnoses. Then Hamilton Depression Rating Scale (HDRS), Hamilton Anxiety Rating Scale (HARS), Panic Disorder Severity Scale (PDSS) and Clinical Global Impression Scale (CGI-S) were applied to participants. Twenty four hour Holter ECG outcomes were analyzed on a computer program and time domain parameters were evaluated. Results: Among the parameters analyzed from HRV, SDANN was significantly higher (p <0.001); duration of RMSSD, NN50 and pNN50 were lower in PD group than the control group (p = 0.003, p = 0.005, p = 0.047, respectively). In the correlation analysis, there was a moderate negative correlation between CGI-S and NN50 and pNN50. In logistic regression analysis, the increase in SDNN was found to increase the probability of PD by 1.11 (95% CI, 1.010-1.209); the increase in SDANN was found to decrease the probability of PD by 0.892 (95% CI, 0.818-0.973), and the increase in pNN50 was found to decrease the probability of PD by 0.523 (95% CI, 0.342-0.801). Conclusion: The data obtained in our study confirm that there is a decrease in some HRV parameters like RMSSD, NN50 and pNN50 reflecting parasympathetic activity among patients with PD.
... In addition to respiratory distress, other prominent symptoms of PD include cardiac symptoms such as chest pain and palpitations. Many studies have reported cardiac differences between PD patients and HC characterized by increased resting heart rate (Larsen et al., 1998;Wilkinson et al., 1998;Friedman and Thayer, 1998;Cohen et al., 2000;Cuthbert et al., 2003;Blechert et al., 2007;Garakani et al., 2009;Martinez et al, 2010, Wise et al., 2011, and decreased heart rate variability (HRV) (Friedman and Thayer, 1998;Sloan et al., 1999;Cohen et al., 2000;Gorman and Sloan, 2000;McCraty et al., 2001;Yeragani et al., 1993;Garakani et al., 2009;Melzig et al., 2009;Wise et al., 2011;Hovland et al., 2012). Decreased HRV is a risk factor for increased mortality in patients with cardiovascular disease (Kleiger et al., 1987;Bigger et al., 1992a;1992b;Tsuji et al., 1996;Liao et al., 1997;La Rovere et al., 1998;Gerritsen et al., 2001;Camm et al., 2004), and has been proposed as a marker for cardiac disease (Task Force of the European Society of Cardiology and the North American Society of Pacing Electrophysiology, 1996). ...
... In addition to respiratory distress, other prominent symptoms of PD include cardiac symptoms such as chest pain and palpitations. Many studies have reported cardiac differences between PD patients and HC characterized by increased resting heart rate (Larsen et al., 1998;Wilkinson et al., 1998;Friedman and Thayer, 1998;Cohen et al., 2000;Cuthbert et al., 2003;Blechert et al., 2007;Garakani et al., 2009;Martinez et al, 2010, Wise et al., 2011, and decreased heart rate variability (HRV) (Friedman and Thayer, 1998;Sloan et al., 1999;Cohen et al., 2000;Gorman and Sloan, 2000;McCraty et al., 2001;Yeragani et al., 1993;Garakani et al., 2009;Melzig et al., 2009;Wise et al., 2011;Hovland et al., 2012). Decreased HRV is a risk factor for increased mortality in patients with cardiovascular disease (Kleiger et al., 1987;Bigger et al., 1992a;1992b;Tsuji et al., 1996;Liao et al., 1997;La Rovere et al., 1998;Gerritsen et al., 2001;Camm et al., 2004), and has been proposed as a marker for cardiac disease (Task Force of the European Society of Cardiology and the North American Society of Pacing Electrophysiology, 1996). ...
Panic disorder (PD) is characterized by anticipatory anxiety and panic, both causing physiological arousal. We investigated the differential responses between anticipatory anxiety and panic in PD and healthy controls (HC). Subjects (15 PD and 30 HC) received an injection of a respiratory stimulant, doxapram, with a high rate of producing panic attacks in PD patients, or an injection of saline. PD subjects had significantly higher scores in anxiety and panic symptoms during both conditions. Analysis of heart rate variability (HRV) indices showed higher sympathetic activity (LF) during anticipatory anxiety and panic states, an increase in the ratio of LF/HF during the anticipatory and panic states and a decrease in parasympathetic (HF) component in PD patients. During doxapram PD subjects increased their LF/HF ratio while HC had a reduction in LF/HF. Parasympathetic component of HRV was lower during anticipatory anxiety in PD. In general, PD showed greater sympathetic and psychological responses related to anxiety and sensations of dyspnea, reduced parasympathetic responses during anticipatory and panic states, but no differences in respiratory response. This confirms previous studies showing that PD patients do not have an intrinsic respiratory abnormality (either heightened or dysregulated) at the level of the brain stem but rather an exaggerated fear response.
Copyright © 2015. Published by Elsevier Ireland Ltd.
... 16 One potential explanation proposed for this association is the dysregulation of the autonomic control of the heart, because ANS activity is associated with CVD 17,18 and anxiety disorders. 16 Some studies reported low HRV in patients with panic disorder (PD), 19,20 while others found that patients with generalized anxiety disorder (GAD) exhibited an increased HR and decreased cardiac vagal tone during rest, as compared to the controls. [21][22][23] One might wonder whether the comorbid diagnosis of anxiety disorders in MDD patients is associated with a greater reduction in HRV as compared with MDD patients without any comorbidity. ...
... One potential explanation was the cumulative effect, that is, a combination of the psychophysiological impact of MDD and anxiety disorders. Previous research showed that both GAD 22,23 and PD 19,20 were associated with decreased HRV. A plausible scenario could be that MDD patients, with any comorbid anxiety disorder, would have a greater reduction in HRV than those with only MDD diagnosis. ...
Objective: Decreased heart rate variability (HRV) has been reported in persons with major depressive disorder (MDD), but the
results obtained are inconsistent. Little is known about the impact of comorbid anxiety disorders on HRV in MDD patients. Both
issues necessitate further investigation. Materials and Methods: Forty-nine unmedicated, physically healthy, MDD patients
without comorbidity, 21 MDD patients with comorbid generalized anxiety disorder (GAD), 24 MDD patients with comorbid
panic disorder (PD), and 81 matched controls were recruited. The Hamilton Depression Rating Scale and the Hamilton Anxiety
Rating Scale are employed to assess the severity of depression and anxiety, respectively. The cardiac autonomic function
was evaluated by measuring the HRV parameters. The frequency-domain indices of HRV were obtained. Results: MDD
patients without comorbidity had lower high-frequency (HF)-HRV (which reflected vagal control of HRV) than controls.
Any comorbid anxiety disorder (GAD or PD) was associated with significantly faster heart rates, relative to the controls, and
caused greater reductions in HF-HRV among MDD patients. MDD participants with comorbid GAD displayed the greatest
reductions in HF-HRV, relative to controls. Correlation analyses revealed that the severity of both depression and anxiety were
significantly associated with the mean R wave to R wave (R-R) intervals, variance, low-frequency (LF)-HRV, and HF-HRV.
Conclusion: The present results show decreased HRV in MDD patients, suggesting that reduction in HRV is a psychophysiological
marker of MDD. MDD patients with comorbid GAD had the greatest reductions in HRV. Further investigation of the links
between MDD and comorbid GAD, HRV, and cardiovascular disease is warranted.
... Investigations concerning resting HRV in PD have revealed inconsistent results. For example, some studies found reduced HRV in PD patients but not in controls (Yeragani et al., 1993;Middleton and Ashby, 1995;Garakani et al., 2009;Wise et al., 2011). While other studies reported no differences in resting HRV between PD patients and controls (Ito et al., 1999;Kikuchi et al., 2009). ...
... First, drug-naive PD patients had significantly lower HRV than controls. Our findings corroborated the findings of earlier studies (Yeragani et al., 1993;Middleton and Ashby, 1995;Garakani et al., 2009;Wise et al., 2011), suggesting that reduction in HRV is a psychophysiological marker of PD. We believe our findings to be reliable because our study had four important strengths: (i) We excluded subjects with psychiatric and physical comorbidities that could potentially confound the association between PD and cardiac autonomic functions. ...
Cardiac autonomic dysregulation has been proposed in panic disorder (PD), but the results are mixed. Analyses with larger sample sizes and better methodology are needed.
Forty-eight drug-naïve individuals with PD and 202 healthy volunteers were recruited for a case-control analysis. We used the Hamilton Anxiety Rating Scale and the Beck Anxiety Inventory to assess anxiety severity. Cardiac autonomic function was evaluated by measuring heart rate variability (HRV) parameters. Frequency-domain indices of HRV were obtained. The obtained results were evaluated in association with personality traits assessed by the Tridimensional Personality Questionnaire.
Patients exhibited reduced mean RR interval (816.94 ± 135.92 versus 873.47 ± 143.36 ms, P = 0.014) and HRV levels (Var 6.37 ± 1.32 versus 7.38 ± 0.95, LF 4.90 ± 1.63 versus5.82 ± 1.11 and HF 4.57 ± 1.53 versus 5.62 ± 1.24 [ln(ms2)], all P < 0.001) as compared to controls, which mainly suggested a reduction in cardiac vagal control in PD. The anxiety severity was negatively correlated with HRV levels (r = -0.29 for Var, r = -0.22 for LF and r = -0.28 for HF, all P < 0.001). The harm avoidance score (which has been suggested to be associated with serotonergic activity) was associated with decreased HRV levels (r = -0.22 for Var, P < 0.01, r = -0.14 for LF, P < 0.05 and r = -0.17 for HF, P < 0.01).
This study demonstrates that PD is associated with cardiac autonomic dysregulation, highlighting the importance of assessing HRV in PD patients.
... Again, reduced Alpha-1 spectral power, attributed to reduced awareness and to increased processing of non-specific information was recorded. Importantly, these EEG changes were associated with vegetative disturbances, including increased mean heart ratio and impaired skin conductance response [33]. Other results were provided by Hanaok et al. with PD patients, as compared with healthy subjects, who manifested lower coherence values with significant differences in F3-F4, C3-C4, P3-P4, F7-T5 and F8-T6 recordings and the intensity of these changes correlated well with disease duration and the severity of panic attacks [34]. ...
Background:
Both the global COVID-19 pandemic situation, as well as the current political situation in Eastern Europe may exacerbate anxiety and contribute to stress-related disorders such as panic disorder. Electroencephalography (EEG)-based neurofeedback provides both assessment of the subject's brainwave activity as well as the possibility of its therapeutic correction. It is possible that it can be implemented as an auxiliary treatment in panic disorders of different origin. The aim of this feasibility study was to demonstrate (both short- and long-term) effectiveness of neurofeedback therapy in a patient with previously diagnosed panic attacks, related to fear of COVID-19 infection.
Methods:
We report the case study of a 47-year-old man affected by panic attacks, related to his profound, constant fear of COVID-19 infection and its sequelae. For the initial diagnostic workup, several clinical and research tools were used: 1. Baseline psychological exam; 2. Anxiety-targeted interview performed by miniQEEG therapist; 3. Analysis of previous clinical test results (EEG record/lab blood test); and 4. The miniQEEG exam (central strip recording Cz-C3-C4), The patient was subjected to regular EEG Neurofeedback sessions for two consecutive months. After completing the treatment, follow-up tests, as listed above were repeated immediately after completing the whole treatment program, as well as 1 and 2 years later. MiniQEEG results were compared with healthy control (age-matched male subject not affected with panic attacks) and evaluated over the time that the subject was involved in the study.
Results:
Initially, the patient was suffering from severe panic attacks accompanied by vegetative symptoms and from destructive and negative thoughts. After 8 consecutive weeks of treatment encompassing sixteen QEEG neurofeedback training sessions (each lasting 30 min), a subjective improvement of his complaints was reported. More importantly, QEEG records of the patient also improved, approximating the pattern of QEEG recorded in the healthy control.
Conclusion:
In this single case-based feasibility analysis, we demonstrate that systematic application of QEEG-Neurofeedback may result in manifest and durable therapeutic effect. Of note, use of this treatment may be a valuable option for patients with panic attack/panic disorder, especially if related to the psychological burden of the COVID-19/war era. Future studies on a larger patient population, especially with a longitudinal/prospective design, are warranted.
... Again, converging evidence suggests that both components of anxiety are reflected in the characteristics of qEEG phenotypes [497,[649][650][651][652][653]. ...
Many practicing clinicians are time-poor and are unaware of the accumulated neuroscience developments. Additionally, given the conservative nature of their field, key insights and findings trickle through into the mainstream clinical zeitgeist rather slowly. Over many decades, clinical, systemic, and cognitive neuroscience have produced a large and diverse body of evidence for the potential utility of brain activity (measured by electroencephalogram—EEG) for neurology and psychiatry. Unfortunately, these data are enormous and essential information often gets buried, leaving many researchers stuck with outdated paradigms. Additionally, the lack of a conceptual and unifying theoretical framework, which can bind diverse facts and relate them in a meaningful way, makes the whole situation even more complex. To contribute to the systematization of essential data (from the authors’ point of view), we present an overview of important findings in the fields of electrophysiology and clinical, systemic, and cognitive neuroscience and provide a general theoretical–conceptual framework that is important for any application of EEG signal analysis in neuropsychopathology. In this context, we intentionally omit detailed descriptions of EEG characteristics associated with neuropsychopathology as irrelevant to this theoretical–conceptual review.
... There was no anxiety effect at the lateral channels but anxiety was associated with significantly higher power centrally, across all frequency bands. These data are consistent with earlier findings with panic disorder patients compared to healthy controls (Wise et al., 2011). At Fz, power difference was generally inversely proportional to frequency, with a modest peak in the alpha range. ...
Anxiety disorders are the most prevalent mental disorders in the world, creating huge economic burdens on health systems and impairing the quality of life for those affected. Recently, ketamine has emerged as an effective anxiolytic even in cases resistant to conventional treatments (TR); but its therapeutic mechanism is unknown. Previous data suggest that ketamine anxiety therapy is mediated by reduced right frontal electroencephalogram (EEG) theta power measured during relaxation. Here we test for a similar theta reduction between population-sample, presumed treatment-sensitive, (TS) anxiety patients and healthy controls. Patients with TS DSM-5 anxiety disorder and healthy controls provided EEG during 10 min of relaxation and completed anxiety-related questionnaires. Frontal delta, theta, alpha1, alpha2, beta, and gamma power, Higuchi’s fractal dimension (HFD) and frontal alpha asymmetry (FAA) values were extracted to match ketamine testing; and we predicted that the controls would have less theta power at F4, relative to the TS anxious patients, and no differences in HFD or FAA. We provide graphical comparisons of our frontal band power patient-control differences with previously published post-pre ketamine TR differences. As predicted, theta power at F4 was significantly lower in controls than patients and FAA was not significantly different. However, HFD was unexpectedly reduced at lateral sites. Gamma power did not increase between controls and patients suggesting that the increased gamma produced by ketamine relates to dissociation rather than therapy. Although preliminary, and indirect, our results suggest that the anxiolytic action of ketamine is mediated through reduced right frontal theta power.
... Anxiety-related arousal can be detected centrally using electroencephalography (EEG), with some evidence that attenuated alpha activity is associated with anxiety (Wise et al., 2011). Increasing alpha magnitude can produce a calming effect in high-anxious individuals (Hardt & Kamiya, 1978). ...
Objective
To investigate the effectiveness of alpha activity neurofeedback training over the parietal lobe in GAD patients.
Methods
Twenty‐six female patients who had been diagnosed as GAD according to the Diagnostic and Statistical Manual of Mental Disorders (5th edition, DSM‐V) criteria were included in this study. Patients were randomized into two groups: the left parietal lobe training group (LPL group, n = 13) and the right parietal lobe training group (RPL group, n = 13), and then received ten 40‐minute alpha training sessions in the relevant area. Evaluations included severity of anxiety (by State‐Trait Anxiety Inventory, STAI) and depression (by Beck Depression Inventory, BDI‐II) after the fifth training session and the last training session.
Results
The scores of STAI‐S decreased significantly two weeks after the fifth training session in both groups (LPL group: from 47.15 ± 10.65 to 38.69 ± 8.78, p<.05; RPL group: from 44.92 ± 12.37 to 37.31 ± 6.41, p < .05) and decreased further at the four weeks’ time point after the last training session (LPL group: 35.15 ± 9.24; RPL group: 29.85 ± 6.18). Compared with baseline, the scores of STAI‐T, BDI‐II and ISI decrease at two weeks, no significant difference found between LPL group and RPL group. The scores of STAI‐T, BDI‐II and ISI decreased at four weeks when compared with two weeks, and no significant difference found between LPL group and RPL group.
Conclusion
Neurofeedback training of alpha activity over the parietal lobe is effective in GAD patients, especially the anxiety trait and depressive symptoms.
... However, the mechanism linking ANS dysfunction and ventricular arrhythmias is not yet fully understood [17]. Several clinical studies have shown an increased incidence of ANS disorders, including increased resting heart rate [18], reduced vagal tone, and increased sympathetic system efficacy [19], in patients with panic disorder compared to healthy controls. HRV is one method used to evaluate ANS function, which is controlled by parasympathetic and sympathetic cardiac nerves. ...
Background and Objectives: The autonomic nervous system (ANS) is involved in panic disorders. ANS dysfunction has been shown to be associated with ventricular arrhythmia and increased heterogeneity of ventricular repolarization. However, there remains limited evidence of the relationship between panic disorders and ventricular depolarization markers, including the Tp-e interval and Tp-e/QT ratio. This study aimed to evaluate ventricular repolarization parameters in patients with panic disorder. Materials and Methods: In total, 40 patients with panic disorder, diagnosed using the Diagnostic and Statistical Manual of Mental Disorders (DSM-5) criteria, were included in the study group. The control group comprised of 50 age-and sex-matched healthy individuals. A standard 12 lead electrocardiogram was recorded on all participants, and heart rate, QT interval, QRS duration, Tp-e interval, and Tp-e/QT ratio were measured. Results: QRS durations and QT intervals were similar in the study and control groups. Compared to the control group, QTd, Tp-e, and cTp-e intervals as well as Tp-e/QT and Tp-e/QTc ratios were significantly increased in patients with panic disorder (p < 0.05 for all). In the study group, the Severity Measure for Panic Disorder-Adult score had a significant positive correlation with the Tp-e interval (r = 0.369, p < 0001), cTp-e interval (r = 0.531, p < 0.001), Tp-e/QT ratio (r = 0.358, p = 0.001), and Tp-e/QTc ratio (r = 0.351, p = 0.001). Conclusion: These findings indicate that panic disorders are associated with increased ventricular repolarization heterogeneity, which may be attributed to ANS dysregulation.
... Park et al. [58] observed an increase of the beta waves at the left temporal lobe when the users experienced fear. The work of [59] showed reduced beta power in the bilateral temporal and right frontal cortex for individuals suffering from panic disorders. An increase of beta intensity in the left temporal lobe was also noticed in [58] whenever the subjects felt threatened. ...
In this paper, we investigate various machine learning classifiers used in our Virtual Reality (VR) system for treating acrophobia. The system automatically estimates fear level based on multimodal sensory data and a self-reported emotion assessment. There are two modalities of expressing fear ratings: the 2-choice scale, where 0 represents relaxation and 1 stands for fear; and the 4-choice scale, with the following correspondence: 0—relaxation, 1—low fear, 2—medium fear and 3—high fear. A set of features was extracted from the sensory signals using various metrics that quantify brain (electroencephalogram—EEG) and physiological linear and non-linear dynamics (Heart Rate—HR and Galvanic Skin Response—GSR). The novelty consists in the automatic adaptation of exposure scenario according to the subject’s affective state. We acquired data from acrophobic subjects who had undergone an in vivo pre-therapy exposure session, followed by a Virtual Reality therapy and an in vivo evaluation procedure. Various machine and deep learning classifiers were implemented and tested, with and without feature selection, in both a user-dependent and user-independent fashion. The results showed a very high cross-validation accuracy on the training set and good test accuracies, ranging from 42.5% to 89.5%. The most important features of fear level classification were GSR, HR and the values of the EEG in the beta frequency range. For determining the next exposure scenario, a dominant role was played by the target fear level, a parameter computed by taking into account the patient’s estimated fear level.
... The amplitude of ongoing EEG activity, particularly in the alpha band (7)(8)(9)(10)(11)(12)(13), is known to be related to fluctuations in attentional response [86,101,11], orienting reaction (OR) [95,8], memory operations with synchronised alpha activity (large amplitudes in the scalp EEG) during the retention of a memory scanning task [51], enhanced recognition of relevant information whilst supressing irrelevant content [51], and general psychophysiological state of a person whereas increased alpha is linked to decreased vigilance and anxious arousal, lowered heart rate and skin conductance levels, and general feeling of relaxation [22,73,114,88], indicating a parasympathetic shift. From this brief overview one may easily see how alpha rhythm that is increased by horizontal EMs could represent an extremely useful mechanism to explain the whole totality of various positive effects of EMDR therapy as well as bridge different theoretical accounts of EMDR: (i) holding a traumatic image in mind (retention) while performing EMs decreases vividness and emotionality of disturbing memories [3,50,105] resulting from a discrepancy between the control of EMs and deployment of attention on the retention [71]; (ii) reconsolidation of memory structures through mechanism of active inhibition [51]; (iii) EMs trigger an orienting response that facilitates access to the traumatic memory without avoidance, causing subsequent rapid relaxation after registering no actual immediate threats [6]; (iv) decrease of heart rate and galvanic skin response as a function of EMs/EMDR [113,24]; (v) increased recognition of accurate information and attentional flexibility [23]; (vi) spontaneous generation of positive insight [56]; (vii) reduced anxious arousal when associated with the traumatic memory [93] similar to processes of memory consolidation via the integration of emotionally charged autobiographical memories into general semantic networks during rapid eye movement (REM) sleep [97,98]. ...
Eye Movement Desensitization and Reprocessing (EMDR) therapy is included in many international trauma treatment guidelines and is also shortlisted as an evidence-based practice for the treatment of psychological trauma and Post-Traumatic Stress Disorder (PTSD). However, its neurobiological mechanisms have not yet been fully understood. In this brief article we propose a hypothesis that a recently introduced neurophysiologically based three-dimensional construct model for experiential selfhood may help to fill this gap by providing the necessary neurobiological rationale of EMDR. In support of this proposal we briefly overview the neurophysiology of eye movements and the triad selfhood components, as well as EMDR therapy neuroimaging studies.
... Other disorders such as bipolar disorder El-Badri et al., 2001;Bas¸ar et al., 2012;Kam et al., 2013;Narayanan et al., 2014;Moeini et al., 2015), anxiety (Sachs et al., 2004;Oathes et al., 2008;Xing et al., 2017) and panic disorder (Knott et al., 1996;Gordeev, 2008;Wise et al., 2011;de Carvalho et al., 2015) are included here for completeness. However generally there was no more than one or two studies for any one condition (eyes closed, eyes open, relative power, absolute power), which was too few for the inference of any trends or for the calculation of consistency scores. ...
A significant proportion of the electroencephalography (EEG) literature focuses on differences in historically pre-defined frequency bands in the power spectrum that are typically referred to as alpha, beta, gamma, theta and delta waves. Here, we review 184 EEG studies that report differences in frequency bands in the resting state condition (eyes open and closed) across a spectrum of psychiatric disorders including depression, attention deficit-hyperactivity disorder (ADHD), autism, addiction, bipolar disorder, anxiety, panic disorder, post-traumatic stress disorder (PTSD), obsessive compulsive disorder (OCD) and schizophrenia to determine patterns across disorders. Aggregating across all reported results we demonstrate that characteristic patterns of power change within specific frequency bands are not necessarily unique to any one disorder but show substantial overlap across disorders as well as variability within disorders. In particular, we show that the most dominant pattern of change, across several disorder types including ADHD, schizophrenia and OCD, is power increases across lower frequencies (delta and theta) and decreases across higher frequencies (alpha, beta and gamma). However, a considerable number of disorders, such as PTSD, addiction and autism show no dominant trend for spectral change in any direction. We report consistency and validation scores across the disorders and conditions showing that the dominant result across all disorders is typically only 2.2 times as likely to occur in the literature as alternate results, and typically with less than 250 study participants when summed across all studies reporting this result. Furthermore, the magnitudes of the results were infrequently reported and were typically small at between 20% and 30% and correlated weakly with symptom severity scores. Finally, we discuss the many methodological challenges and limitations relating to such frequency band analysis across the literature. These results caution any interpretation of results from studies that consider only one disorder in isolation, and for the overall potential of this approach for delivering valuable insights in the field of mental health.
... Nonetheless, cortical dynamics may be altered at specific time points in the menstrual cycle, as indicated by interhemispheric transfer time (131), attentional blink (138) and resting state alpha oscillation (41). Of these observations, the latter is particularly compelling, as hemispheric asymmetry in the alpha band has been identified in numerous psychiatric conditions, including depression (63,134), social anxiety disorder (208), panic disorder (352), and PMDD (10,172). A model by Davidson (61) describes this phenomenon as a result of lateralization of emotion processing, wherein positive emotions activate the left PFC, and negative emotions the right. ...
In this article, we examine evidence supporting the role of reproductive steroids in the regulation of mood and behavior in women and the nature of that role. In the first half of the article, we review evidence for the following: (i) the reproductive system is designed to regulate behavior; (ii) from the subcellular to cellular to circuit to behavior, reproductive steroids are powerful neuroregulators; (iii) affective disorders are disorders of behavioral state; and (iv) reproductive steroids affect virtually every system implicated in the pathophysiology of depression. In the second half of the article, we discuss the diagnosis of the three reproductive endocrine-related mood disorders (premenstrual dysphoric disorder, postpartum depression, and perimenopausal depression) and present evidence supporting the relevance of reproductive steroids to these conditions. Existing evidence suggests that changes in reproductive steroid levels during specific reproductive states (i.e., the premenstrual phase of the menstrual cycle, pregnancy, parturition, and the menopause transition) trigger affective dysregulation in susceptible women, thus suggesting the etiopathogenic relevance of these hormonal changes in reproductive mood disorders. Understanding the source of individual susceptibility is critical to both preventing the onset of illness and developing novel, individualized treatments for reproductive-related affective dysregulation. (C) 2016 American Physiological Society.
... Alpha asymmetry also predicted trait anxiety one year later (Blackhart, Minnix, & Kline, 2006). Furthermore, altered alpha asymmetry has been shown in patients with a panic disorder (Wiedemann et al., 1999;Wise, McFarlane, Clark, & Battersby, 2011), social phobia posttraumatic stress disorder , and depression with (Bruder et al., 1997) and without (Allen & Kline, 2004;Henriques & Davidson, 1991;Kemp et al., 2010) co-morbid anxiety disorder. Studies in OCD patients are scarce as yet, with inconsistent results. ...
Trotz zahlreicher Untersuchungen lässt sich bei der Zwangsstörung noch kein einheitliches, alle Befunde integrierendes Krankheitsmodell formulieren. Die Verarbeitung von emotionalen Reizen könnte bei Personen mit Zwangsstörungen verändert sein. Dies trägt möglicherweise zur Entwicklung und Aufrechterhaltung der Störung bei. Das Ziel der vorliegenden Arbeit war es, spezifische Komponenten dieser Verarbeitung zu untersuchen. Zuerst wurde in zwei unterschiedlichen Studien überprüft, ob die Orientierung der Aufmerksamkeit zu neuen Reizen bei Patienten mit Zwangsstörungen verstärkt ist. Zu diesem Zweck wurden durch neue Reize evozierte Potentiale im Elektroenzephalogramms (EEG) gemessen. Anschließend wurde in einer Studie überprüft, ob das Verhältnis der Aktivierungen von dem Vermeidungs- zum Annäherungssystem bei den Betroffenen verändert ist. Dies lässt sich an Hand der Ermittlung der hemisphärischen Verteilung von Alpha-Wellen in frontalen Hirnregionen feststellen. Die Ergebnisse der ersten beiden Studien ergaben, dass Patienten unabhängig vom emotionalen Kontext eine stärkere Aufmerksamkeitshinwendung zu neuen Reizen zeigen (Studie 1), was allerdings nicht beobachtet wurde, wenn die neuen Reize innerhalb des Aufmerksamkeitsfokus lagen (Studie 2). Dieses Ergebnis wurde als überaktives Gefahrenerkennungssystem bei Patienten interpretiert. Weiterhin ließ sich feststellen, dass Patienten im Vergleich zu gesunden Kontrollen in frontalen Hirnregionen eine Verlagerung der Alpha Asymmetrie zur linken Gehirnhemisphäre aufwiesen (Studie 3). Dieser Befund wurde unabhängig von einer Stimulierung durch emotionale Reize gemacht. Er lässt sich als stärkere Aktivierung des Vermeidungs- im Verhältnis zum Annäherungssystem deuten. Zusammengefasst zeigte sich bei Patienten mit Zwangsstörungen eine veränderte Verarbeitung von emotionalen Reizen. Aus diesen Befunden können spezifische Empfehlungen für die Behandlung der Störung abgeleitet werden.
... Despite the few studies, the alpha band decreased activity and the beta band increased activity have been a pattern for PD patients (Wiedemann et al., 1998;Gordeev, 2008;Wise et al., 2011). The alpha band (8-13 Hz) reflects top-down, inhibitory control processes. ...
... In another study, patients with panic disorders show a reduction in alpha power and lower mean RR interval and higher LF/HF ratio when compared with healthy controls. 30 In our current study, there was a significant decrease in alpha, theta and beta power and a significant concomitant decrease in HF and increase LF/HF ratio. These results suggest that autonomic changes induced by Mozart music stimuli might be mediated through the central nervous system. ...
Objective
Listening to Mozart K.448 has been demonstrated to improve spatial task scores, leading to what is known as the Mozart Effect. However, most of these reports only describe the phenomena but lack the scientific evidence needed to properly investigate the mechanism of Mozart Effect. In this study, we used electroencephalography (EEG) and heart rate variability (HRV) to evaluate the effects of Mozart K.448 on healthy volunteers to explore Mozart Effect.
Design
An EEG-based post-intervention analysis.
Setting
Kaohsiung Medical University Hospital, Kaohsiung, Taiwan.
Participants
Twenty-nine college students were enrolled. They received EEG and electrocardiogram examinations simultaneously before, during and after listening to the first movement of Mozart K.448.
Main outcome measure
EEG alpha, theta and beta power and HRV were compared in each stage.
Results
The results showed a significant decrease in alpha, theta and beta power when they listened to Mozart K.448. In addition, the average root mean square successive difference, the proportion derived by dividing NN50 by the total number of NN intervals, standard deviations of NN intervals and standard deviations of differences between adjacent NN intervals showed a significant decrease, while the high frequency revealed a significant decrease with a significantly elevated low-frequency/high-frequency ratio.
Conclusion
Listening to Mozart K.448 significantly decreased EEG alpha, theta and beta power and HRV. This study indicates that there is brain cortical function and sympathetic tone activation in healthy adults when listening to Mozart K.448, which may play an important role in the mechanism of Mozart Effect.
... Differences from normal in the HRV signal time/frequency structure emerge at early stages [132]; a negative relationship between anxiety traits and HRV descriptors of vagal control has been described, with the LF/HF ratio positively correlating with anxiety symptoms [133,134]. Desynchronization of the EEG power in the 8-11Hz frequency interval has been associated with reduced HRV responses in panic disorder [135]. ...
Heart rate variability (HRV) measures are established indices of the sympathetico-parasympathetic balance in cardiovascular research. HRV descriptors are thought to indirectly reflect complex patterns of brain activation as well and are deemed capable of providing information on the CNS
functional organization and the bidirectional interaction between the CNS and the autonomic nervous system (ANS). Current integrative models equate HRV to CNS/ANS outputs, with HRV reflecting affective, physiological, “cognitive” and behavioral elements, and homeostatic responses. Clinical
application is in the study of patients with psychiatric disorders, traumatic brain injury, pain, disorder of consciousness, endocrine or metabolic disorders, impaired emotion-specific processing, personality and communication disorders, epilepsy. HRV provides researchers with physiological measures also in the absence of conscious behavior or whenever complex experimental conditions and data collection are impracticable, e.g. in intensive care units.
... Lower right compared to left frontal alpha power was found in nonclinical samples of high-anxious in comparison to low-anxious participants (Mathersul, Williams, Hopkinson, & Kemp, 2008). Furthermore, altered alpha distribution with relatively lower right hemisphere power has been shown in patients diagnosed with panic disorder (Wiedemann et al., 1999;Wise, McFarlane, Clark, & Battersby, 2011), social phobia (Moscovitch et al., 2011), posttraumatic stress disorder (Rabe, Beauducel, Zollner, Maercker, & Karl, 2006), and depression with (Bruder et al., 1997) and without (Kemp et al., 2010) comorbid anxiety disorder. ...
Hemispheric topography of alpha band power in the electroencephalogram has been linked to approach/avoidance motivation and may index the risk for anxiety disorders and depression. We quantified lower alpha band power (8-10 Hz) in 20 patients with obsessive-compulsive disorder (OCD) and 20 matched healthy controls during blocks of rest and presentation of neutral, aversive, and OCD-related pictures. Compared to the control group, OCD patients showed altered asymmetry, with frontal alpha power in the 8-10 Hz band being more dominant in the left hemisphere across all conditions. This alteration was not observed over parietal areas, and also did not show in the upper alpha, and the theta and beta bands. This change in hemispheric topography of lower alpha band power supports the hypothesis of relatively increased avoidance motivation in OCD. Altered asymmetry appears to be traitlike in OCD, suggesting a link to depressive disorders.
... Despite the few studies, the alpha band decreased activity and the beta band increased activity have been a pattern for PD patients (Wiedemann et al., 1998;Gordeev, 2008;Wise et al., 2011). The alpha band (8-13 Hz) reflects top-down, inhibitory control processes. ...
Panic attacks are thought to be a result from a dysfunctional coordination of cortical and brainstem sensory information leading to heightened amygdala activity with subsequent neuroendocrine, autonomic and behavioral activation. Prefrontal areas may be responsible for inhibitory top-down control processes and alpha synchronization seems to reflect this modulation. The objective of this study was to measure frontal absolute alpha-power with qEEG in 24 subjects with panic disorder and agoraphobia (PDA) compared to 21 healthy controls.
qEEG data were acquired while participants watched a computer simulation, consisting of moments classified as "high anxiety"(HAM) and "low anxiety" (LAM). qEEG data were also acquired during two rest conditions, before and after the computer simulation display.
We observed a higher absolute alpha-power in controls when compared to the PDA patients while watching the computer simulation. The main finding was an interaction between the moment and group factors on frontal cortex. Our findings suggest that the decreased alpha-power in the frontal cortex for the PDA group may reflect a state of high excitability.
Our results suggest a possible deficiency in top-down control processes of anxiety reflected by a low absolute alpha-power in the PDA group while watching the computer simulation and they highlight that prefrontal regions and frontal region nearby the temporal area are recruited during the exposure to anxiogenic stimuli.
... There is also evidence for functionally altered cortical structures during resting state in PD: studies have mostly but not consistently (e.g., Koh et al. 2010) discerned reduced activation in the frontal cortex (De Cristofaro et al. 1993;Eren et al. 2002Eren et al. , 2003Nordahl et al. 1998Nordahl et al. , 1990 and in temporal (Bisaga et al. 1998;Lee et al. 2006) and parietal areas (Bisaga et al. 1998;Nordahl et al. 1990). There is also support for frontal EEG a asymmetry (Wiedemann et al. 1999;Wise et al. 2011) and differences in right temporal a power (Bystritsky et al. 1999). Furthermore, increased activation in the thalamus, cerebellum, midbrain, and brain stem has been found (Sakai et al. 2005), with, however, also null-findings (Lucey et al. 1997a, b). ...
In 2000, Gorman et al. published a widely acknowledged revised version of their 1989 neuroanatomical hypothesis of panic disorder (PD). Herein, a 'fear network' was suggested to mediate fear- and anxiety-related responses: panic attacks result from a dysfunctional coordination of 'upstream' (cortical) and 'downstream' (brainstem) sensory information leading to heightened amygdala activity with subsequent behavioral, autonomic and neuroendocrine activation. Given the emergence of novel imaging methods such as fMRI and the publication of numerous neuroimaging studies regarding PD since 2000, a comprehensive literature search was performed regarding structural (CT, MRI), metabolic (PET, SPECT, MRS) and functional (fMRI, NIRS, EEG) studies on PD, which will be reviewed and critically discussed in relation to the neuroanatomical hypothesis of PD. Recent findings support structural and functional alterations in limbic and cortical structures in PD. Novel insights regarding structural volume increase or reduction, hyper- or hypoactivity, laterality and task-specificity of neural activation patterns emerged. The assumption of a generally hyperactive amygdala in PD seems to apply more to state than trait characteristics of PD, and involvement of further areas in the fear circuit, such as anterior cingulate and insula, is suggested. Furthermore, genetic risk variants have been proposed to partly drive fear network activity. Thus, the present state of knowledge generally supports limbic and cortical prefrontal involvement as originally proposed in the neuroanatomical hypothesis. Some modifications might be suggested regarding a potential extension of the fear circuit, genetic factors shaping neural network activity and neuroanatomically informed clinical subtypes of PD potentially guiding future treatment decisions.
Background: No study has yet to simultaneously compare generalized anxiety disorder (GAD), panic disorder (PD), and social anxiety disorder (SAD) with respect to restingstate functional connectivity (rsFC) and anxiety symptom severity.
Methods: We collected articles from PubMed, PsycINFO, and ScienceDirect and subjected articles to seven eligibility criteria to be considered for inclusion. Included articles were screened using the QUADAS-2 to assess article quality. Articles were also subjected to a forest plot, activation likelihood estimation (ALE) meta-analysis, and a multiple regression to measure the effect of anxiety symptom severity and rsFC between conditions. We also subjected our sample to a funnel plot with Egger's test to determine publication bias.
Results: Our initial search yielded 1022 studies. After eligibility criteria we retained 30 articles. Quality assessment indicated no major issues with bias or applicability. Our forest plot indicated that all conditions showed a robust effect on anxiety symptom severity when compared with controls. Our ALE meta-analysis showed convergent intranetwork rsFC within the default mode network (DMN) across conditions. Our multiple regression indicated that all conditions exhibited very strong correlations between DMN connectivity and anxiety symptom severity. Funnel plot and Egger's test indicated no presence of publication bias.
Limitations: Our sample was limited by the following: No longitudinal data, no specific time series neuroimaging data, some biased demographic data, and the possibility that some studies might have been missed during review.
Conclusion: GAD, PD, and SAD appear to exhibit increased intranetwork connectivity in the DMN which correlates with increased severity of anxiety symptoms.
Objective:
Panic disorder (PD) may cause serious cardiac arrhythmias by causing electrical abnormalities. Abnormal P-wave axis (aPwa), presence of fragmented QRS (fQRS), widen frontal QRS-T angle (fQRSTa), QRS duration corrected (QRSdc) and log/logQRS duration/RR interval (log/logQRS/RR) have been correlated with an increased risk of serious supraventricular and ventricular cardiac arrhythmias in a general population. The aim of this study was to determine these newly explored atrial and ventricular arrhythmia indicators in patients with PD compared with healthy subjects.
Method:
A total of 169 newly diagnosed PD patients and 128 healthy subjects were included in the study. Panic and Agoraphobia Scale (PAS) was administered and 12-lead electrocardiography (ECG) measurements were obtained. Electrocardiographic parameters including aPwa, fQRSTa, presence of fQRS, QRS duration corrected (QRSdc), log/logQRS duration/RR distance (log/logQRS/RR) were compared between the two groups.
Results:
The prevalence of aPwa and fQRS, in addition to fQRSTa, QRSdc, and log/logQRS/RR ratio values were significantly increased in the PD group compared to the healthy controls. Correlation analyses revealed that wider fQRSTa, number of fQRS derivation, number of total fQRS, wider QRSdc, and log/logQRS/RR ratio significantly correlated with PDSS. Logistic regression analysis results showed that fQRSTa and the number of total fQRS were independently associated with PD.
Conclusion:
PD is associated with wider fQRSTa, QRSdc and log/logQRS/RR in addition to the increased prevalence of abnormal aPwa and presence of fQRS. Therefore, this study suggests that untreated PD patients are susceptible to supraventricular in ventricular arrhythmia, indicating that ECG should be routinely obtained in the management of PD patients.
The current study aimed to investigate the possibility of rapid and accurate diagnoses of Panic disorder (PD) and Major depressive disorder (MDD) using machine learning. The support vector machine method was applied to 2-channel EEG signals from the frontal lobes (Fp1 and Fp2) of 149 participants to classify PD and MDD patients from healthy individuals using non-linear measures as features. We found significantly lower correlation dimension and Lempel-Ziv complexity in PD patients and MDD patients in the left hemisphere compared to healthy subjects at rest. Most importantly, we obtained a 90% accuracy in classifying MDD patients vs. healthy individuals, a 68% accuracy in classifying PD patients vs. controls, and a 59% classification accuracy between PD and MDD patients. In addition to demonstrating classification performance in a simplified setting, the observed differences in EEG complexity between subject groups suggest altered cortical processing present in the frontal lobes of PD patients that can be captured through non-linear measures. Overall, this study suggests that machine learning and non-linear measures using only 2-channel frontal EEGs are useful for aiding the rapid diagnosis of panic disorder and major depressive disorder.
The aim of the present study was to examine self-report, peripheral nervous system, and central nervous system correlates of naturally-occurring, chronic hyperventilation (HV, assessed by hypocapnia or low resting state low end-tidal CO2), and to examine the additional effect of acute, experimentally-induced HV in anxious and healthy participants. By identifying the biomarkers of anxiety-related chronic HV and examining responses to acute HV, we hope to identify meaningful, mechanistic targets for further treatment development. Seventy anxious patients and 34 healthy control participants completed electroencephalogram (EEG) and peripheral nervous system recording at baseline and following a paced breathing task. Diagnosis x baseline hypnocapnia group analyses indicated that anxious/hypocapnic patients exhibited greater nonspecific skin conductance response amplitude than did anxious/normocapnic patients, and the anxious group reported greater HV-related symptoms and anxiety sensitivity than did the control group. However, no EEG abnormalities were noted as a function of anxiety group or baseline hypocapnia status. Following paced HV, anxious patients (but not controls) exhibited an increase in left-frontal alpha 1 power. Hypocapnic, but not normocapnic, participants exhibited an increase in skin conductance levels. Anxious patients reported an increase in negative cognitive appraisals of HV symptoms, and anxious/hypocapnic participants reported an increase in affective responses to HV. Thus, chronic HV is associated with greater arousal, and increased self-reported and physiological sensitivity to paced HV. Patients who chronically hyperventilate appear to be more sensitive to respiratory distress, responding with higher levels of anxiety and poorer tolerance of the physiological sensations accompanying acute HV.
Recently, interest has grown in the assessment of anxiety that leverages human physiological and behavioral data to address the drawbacks of current subjective clinical assessments. Complex experiences of anxiety vary on multiple characteristics, including triggers, responses, duration and severity, and impact differently on the risk of anxiety disorders. This article reviews the past decade of studies that objectively analyzed various anxiety characteristics related to five common anxiety disorders in adults utilizing features of cardiac, electrodermal, blood pressure, respiratory, vocal, posture, movement and eye metrics. Its originality lies in the synthesis and interpretation of consistently discovered heterogeneous predictors of anxiety and multimodal-multisensor analytics based on them. We reveal that few anxiety characteristics have been evaluated using multimodal-multisensor metrics, and many of the identified predictive features are confounded. As such, objective anxiety assessments are not yet complete or precise. That said, few multimodal-multisensor systems evaluated indicate an approximately 11.73% performance gain compared to unimodal systems, highlighting a promising powerful tool. We suggest six high-priority future directions to address the current gaps and limitations in infrastructure, basic knowledge and application areas. Action in these directions will expedite the discovery of rich, accurate, continuous and objective assessments and their use in impactful end-user applications.
Resting state alpha power asymmetry in frontal and temporal regions has been reported in various clinical populations, possibly indicating deficits in prefrontal control. In panic disorder (PD), results regarding alpha asymmetric activity to date have been mixed. This study compared 55 PD patients and 42 healthy controls (HC) with regards to resting state alpha power asymmetry. Our results show more right-than-left fronto-lateral alpha power in PD, whereas at other sites and in HC no significant differences were detected. These results support the notion of altered neurobiological processes in PD that possibly represent a vulnerability to the experience of panic attacks. Further studies are needed to clarify potential causal implications of this finding in the genesis of PD, as well as to specify the functional significance of fronto-lateral alpha power asymmetry in PD.
Heart rate variability (HRV), a measure of the variability in intervals between subsequent heart beats, is now widely considered an index of emotion regulatory capacity and the ability to adapt flexibly to changing environmental demands. Abnormalities in HRV are implicated in a host of psychopathologies, making it a potentially powerful transdiagnostic biobehavioral change mechanism in treatment interventions. While most mental illnesses are associated with low HRV, eating disorders have been linked to elevated HRV. We examined 62 research articles on HRV in psychopathology to test the hypothesis that there is an “ideal range” of HRV that predicts optimal functioning. Relationships between symptom severity and parameters that quantify HRV were examined graphically. More extreme time-domain HRV measures, both high and low, were associated with psychopathology, whereas healthy controls displayed mid-range values. Findings preliminarily support the hypothesis that there is an “ideal range” of HRV that could be targeted in biofeedback interventions.
Background:
Autonomic nervous system (ANS) dysfunction is a putative underlying mechanism for increased cardiovascular disease risk in individuals with psychiatric disorders. Previous studies suggest that this risk may be related to psychotropic medication use. In the present study we systematically reviewed and analyzed published studies of heart rate variability (HRV), measuring ANS output, to determine the effect of psychiatric illness and medication use.
Methods:
We searched for studies comparing HRV in physically healthy adults with a diagnosed psychiatric disorder to controls and comparing HRV pre- and post-treatment with a psychotropic medication.
Results:
In total, 140 case-control (mood, anxiety, psychosis, dependent disorders, k = 151) and 30 treatment (antidepressants, antipsychotics; k = 43) studies were included. We found that HRV was reduced in all patient groups compared to controls (Hedges g = -0.583) with a large effect for psychotic disorders (Hedges g = -0.948). Effect sizes remained highly significant for medication-free patients compared to controls across all disorders. Smaller and significant reductions in HRV were observed for specific antidepressants and antipsychotics.
Limitations:
Study quality significantly moderated effect sizes in case-control analyses, underscoring the importance of assessing methodological quality when interpreting HRV findings.
Conclusion:
Combined findings confirm substantial reductions in HRV across psychiatric disorders, and these effects remained significant even in medication-free individuals. Reductions in HRV may therefore represent a significant mechanism contributing to elevated cardiovascular risk in individuals with psychiatric disorders. The negative impact of specific medications on HRV suggest increased risk for cardiovascular disease in these groups, highlighting a need for treatment providers to consider modifiable cardiovascular risk factors to attenuate this risk.
Clinical, psychometric, neuropsychological, and neurophysiological methods (quantitative EEG and P300 auditory event-related potentials) were used to study 22 patients with panic disorder without agoraphobia, 19 patients with the paroxysmal form of atrial fibrillation, and 43 healthy subjects. Patients with panic disorder differed from patients with paroxysmal atrial fibrillation in having higher levels of anxiety and greater impairments to cognitive functions. As compared with healthy subjects, patients with panic disorder showed greater P300 peak amplitude and EEG spectral power in the theta and beta frequency ranges in the right hemisphere; P300 peak amplitude and EEG spectral power in the beta frequency range in both hemispheres were decreased in paroxysmal atrial fibrillation. These data may provide evidence that different mechanisms may underlie the occurrence of paroxysmal states of neurotic (panic disorder) and psychosomatic (paroxysmal atrial fibrillation) nature.
The efficacy of cognitive-behavioral therapy (CBT) for pediatric obsessive-compulsive disorder (OCD) has been the subject of much study over the past fifteen years. Building on a foundation of case studies and open clinical trials, the literature now contains many methodologically sound studies that have compared full CBT protocols to waitlist controls, pill placebo, psychosocial comparison conditions, active medication, combined treatments, and brief CBT. This review is part of a series commissioned by The Canadian Institute for Obsessive Compulsive Disorders (CIOCD) in an effort to publish in one place what is known about the efficacy of treatments for OCD. A total of fourteen studies were identified; collectively their findings support the efficacy of CBT for youth with OCD. CBT protocols that emphasized either strictly behavioral or cognitive conceptualizations have each been found efficacious relative to waitlist controls. Efforts to enhance CBT׳s efficacy and reach have been undertaken. These trials provide guidance regarding next steps to be taken to maximize efficacy and treatment availability. Findings from studies in community clinics suggest that significant treatment benefits can be realized and are not reported only from within academic contexts. These findings bode well for broader dissemination efforts. Recommendations for future research directions are provided.
Copyright © 2015 Elsevier Ireland Ltd. All rights reserved.
Background: Anxiety disorders increase risk of future cardiovascular disease (CVD) and mortality, even after controlling for confounds including smoking, lifestyle, and socioeconomic status, and irrespective of a history of medical disorders. While impaired vagal function, indicated by reductions in heart rate variability (HRV), may be one mechanism linking anxiety disorders to CVD, prior studies have reported inconsistent findings highlighting the need for meta-analysis. Method: Studies comparing resting-state HRV recordings in patients with an anxiety disorder as a primary diagnosis and healthy controls were considered for meta-analysis. Results: Meta-analyses were based on 36 articles, including 2086 patients with an anxiety disorder and 2294 controls. Overall, anxiety disorders were characterized by lower HRV [high frequency (HF): Hedges' g = −0.29. 95% CI: −0.41 to −0.17, p < 0.001; time domain: Hedges' g = −0.45, 95% CI: −0.57 to −0.33, p < 0.001] than controls. Panic disorder (n = 447), post-traumatic stress disorder (n = 192), generalized anxiety disorder (n = 68), and social anxiety disorder (n = 90), but not obsessive–compulsive disorder (n = 40), displayed reductions in HF HRV relative to controls (all ps < 0.001). Conclusion: Anxiety disorders are associated with reduced HRV, findings associated with a small-to-moderate effect size. Findings have important implications for future physical health and well-being of patients, highlighting a need for comprehensive cardiovascular risk reduction.
Background: Anxiety disorders increase risk of future cardiovascular disease (CVD) and mortality, even after controlling for confounds including smoking, lifestyle, and socioeconomic status, and irrespective of a history of medical disorders. While impaired vagal function, indicated by reductions in heart rate variability (HRV), may be one mechanism linking anxiety disorders to CVD, prior studies have reported inconsistent findings highlighting the need for meta-analysis.
Method: Studies comparing resting-state HRV recordings in patients with an anxiety disorder as a primary diagnosis and healthy controls were considered for meta-analysis.
Results: Meta-analyses were based on 36 articles, including 2086 patients with an anxiety disorder and 2294 controls. Overall, anxiety disorders were characterized by lower HRV [high frequency (HF): Hedges’ g = −0.29. 95% CI: −0.41 to −0.17, p < 0.001; time domain: Hedges’ g = −0.45, 95% CI: −0.57 to −0.33, p < 0.001] than controls. Panic disorder (n = 447), post-traumatic stress disorder (n = 192), generalized anxiety disorder (n = 68), and social anxiety disorder (n = 90), but not obsessive–compulsive disorder (n = 40), displayed reductions in HF HRV relative to controls (all ps < 0.001).
Conclusion: Anxiety disorders are associated with reduced HRV, findings associated with a small-to-moderate effect size. Findings have important implications for future physical health and well-being of patients, highlighting a need for comprehensive cardiovascular risk reduction.
Measures of heart rate variability (HRV) are major indices of the sympathovagal balance in cardiovascular research. These measures are thought to reflect complex patterns of brain activation as well and HRV is now emerging as a descriptor thought to provide information on the nervous system organization of homeostatic responses in accordance with the situational requirements. Current models of integration equate HRV to the affective states as parallel outputs of the central autonomic network, with HRV reflecting its organization of affective, physiological, “cognitive,” and behavioral elements into a homeostatic response. Clinical application is in the study of patients with psychiatric disorders, traumatic brain injury, impaired emotion-specific processing, personality, and communication disorders. HRV responses to highly emotional sensory inputs have been identified in subjects in vegetative state and in healthy or brain injured subjects processing complex sensory stimuli. In this respect, HRV measurements can provide additional information on the brain functional setup in the severely brain damaged and would provide researchers with a suitable approach in the absence of conscious behavior or whenever complex experimental conditions and data collection are impracticable, as it is the case, for example, in intensive care units. (PsycINFO Database Record (c) 2012 APA, all rights reserved)
The Approach-Avoidance Task (AAT) measures automatic approach-avoidance tendencies and their regulation: Compatible reactions (approach positive, avoid negative) are faster than incompatible ones (approach negative, avoid positive). The present study assessed event-related potentials (ERPs) in 15 healthy persons for depicting neuropsychological sub-processes of such stimulus-response compatibility (SRC) effects. Early attention allocation preparing efficient stimulus classification (N1 ERP) and response inhibition on the level of response representations (N2 ERP) were found to underlie the solution of the AAT-conflict. For positive stimuli, these processes were enhanced during the incompatible condition avoid positive compared to the compatible condition approach positive. Source localization analysis revealed activity in right occipital areas (N1 ERP), and in left DLPFC and insula (N2 ERP) to be neuronal generators of these electrophysiological SRC effects. This neuronal regulation resulted in no influence of incompatibility at the behavioural level. For negative pictures, we found the reversed pattern: There were no electrophysiological SRC effects, but clear behavioural SRC effects in both RTs and error frequency, i.e. participants were faster and made fewer errors during avoiding than approaching negative pictures. These valence-specific differences are in line with previous studies indicating negative stimuli-probably due to higher importance for survival-to more strongly influence behaviour.
Neural structures involved in social cognition (e.g., amygdala, orbitofrontal cortex) have been implicated in judgements of trustworthiness. These regions are also functionally atypical in individuals with autism spectrum disorders (ASDs). Studies investigating judgements of trustworthiness in ASDs have suggested possible disruptions in the allocation of significance to social stimuli. Concurrent measures of autonomic responses provide further insight into these deficits, given their role in the direction of attention and allocation of significance. Thirty high-functioning adults with ASDs and 31 non-clinical controls viewed neutral images piloted as most "positive" and "negative". Skin conductance (SCR, SCL) and evoked cardiac deceleration (ECD) were recorded. Adults with ASDs did not differ from controls in ratings of trustworthiness. However, they displayed atypical SCRs, providing further support for a disruption in the allocation of emotional significance.
Stress regulation during pregnancy is considered to be connected to the timing of labour initiation. Although increasing knowledge is emerging on the regulation of parturition, there is currently no way to predict the start of spontaneous labour in women. The main aim of this study was to assess pain threshold and the sympathetic nervous system response to cold pain in relation to the onset of labour in healthy pregnant women. Ninety-three pregnant women were recruited and assessed for skin conductance (SC) activity during a cold pressor test in gestational week 38. Pain threshold and cold endurance were also measured and the results were compared with data obtained from hospital records. Seventy-four women had a spontaneous labour onset and a valid SC measurement. SC activity during the cold pressor test decreased significantly with the number of days left to spontaneous parturition. This may indicate a gradual decrease in sympathetic autonomic nervous system reactivity even during the last weeks of pregnancy. Measuring SC activity during mild stress provocation is a rapid and non-invasive means to study variation in sympathetic reactivity during pregnancy, and may be useful in research on stress regulation in pregnancy and its relation to labour initiation.
Hans-Jürgen Eysenck suggested that introverts are characterized by greater cortical arousal or arousability than extraverts. This prediction was tested in several studies that used the electroencephalogram (EEG) to index cortical activity, but the relations between the EEG measures and Extraversion are typically small. Possibly, situational factors that are external to the laboratory may act as nuisance variables and affect cortical activity, thus, mitigating the relation between arousal or arousability and Extraversion. To test this hypothesis, resting EEG was acquired on four occasions of measurement and Extraversion was assessed by questionnaire. A structural equation model (SEM) represented cortical arousal, arousability, and external factors. This analysis suggested that (1) arousal and arousability are independent factors, (2) external factors only marginally contribute to the variance of the EEG measures, and (3) the relations between the EEG measures and Extraversion were insignificant even if external factors were statistically controlled. (PsycINFO Database Record (c) 2012 APA, all rights reserved)
To assess the external validity of laboratory baselines in panic disorder (PD), frequently associated with respiratory pattern abnormalities like increased respiratory variability and sighing, implying a stable pathophysiologic trait characteristic.
Physical activity and a variety of breath-by-breath volumetric, timing, and variability measures of respiration were recorded in the daily life of 26 patients with PD and 26 healthy controls (HC), using a novel ambulatory monitoring system optimized for reliable assessment of respiratory pattern. Data were stratified for physical activity to eliminate its confounding effects.
Groups showed strong and consistent diurnal patterns in almost all respiratory variables. However, patients with PD did not differ from HC regarding any of the respiratory timing, volumetric and variability measures, with negligible group effect sizes for all measures. Patients with fewer self-reported respiratory symptoms of anxiety exhibited more pronounced rapid shallow breathing as well as diminished total breath time and its variability.
Despite state-of-the-art ambulatory assessment and sufficient statistical power to detect respiratory alterations previously observed in the laboratory, we found no evidence for such alterations in PD patients' daily life. Neither the total PD group nor patients with particularly pronounced respiratory symptomatology displayed increased respiratory variability. These results caution against interpreting results from laboratory baselines in PD as reflecting a stable trait characteristic. Rather, they likely represent a state-trait interaction due to enhanced reactivity of PD patients to novel environments. These results challenge aspects of respiratory theories of PD that were based on laboratory findings.
The perceived emotional value of stimuli and, as a consequence the subjective emotional experience with them, can be affected by context-dependent styles of processing. Therefore, the investigation of the neural correlates of emotional experience requires accounting for such a variable, a matter of an experimental challenge. Closing the eyes affects the style of attending to auditory stimuli by modifying the perceptual relationship with the environment without changing the stimulus itself. In the current study, we used fMRI to characterize the neural mediators of such modification on the experience of emotionality in music. We assumed that closed eyes position will reveal interplay between different levels of neural processing of emotions. More specifically, we focused on the amygdala as a central node of the limbic system and on its co-activation with the Locus Ceruleus (LC) and Ventral Prefrontal Cortex (VPFC); regions involved in processing of, respectively, 'low', visceral-, and 'high', cognitive-related, values of emotional stimuli. Fifteen healthy subjects listened to negative and neutral music excerpts with eyes closed or open. As expected, behavioral results showed that closing the eyes while listening to emotional music resulted in enhanced rating of emotionality, specifically of negative music. In correspondence, fMRI results showed greater activation in the amygdala when subjects listened to the emotional music with eyes closed relative to eyes open. More so, by using voxel-based correlation and a dynamic causal model analyses we demonstrated that increased amygdala activation to negative music with eyes closed led to increased activations in the LC and VPFC. This finding supports a system-based model of perceived emotionality in which the amygdala has a central role in mediating the effect of context-based processing style by recruiting neural operations involved in both visceral (i.e. 'low') and cognitive (i.e. 'high') related processes of emotions.
Brain activity is continuously modulated, even at "rest". The alpha rhythm (8-12 Hz) has been known as the hallmark of the brain's idle-state. However, it is still debated if the alpha rhythm reflects synchronization in a distributed network or focal generator and whether it occurs spontaneously or is driven by a stimulus. This EEG/fMRI study aimed to explore the source of alpha modulations and their distribution in the resting brain. By serendipity, while computing the individually defined power modulations of the alpha-band, two simultaneously occurring components of these modulations were found. An 'induced alpha' that was correlated with the paradigm (eyes open/ eyes closed), and a 'spontaneous alpha' that was on-going and unrelated to the paradigm. These alpha components when used as regressors for BOLD activation revealed two segregated activation maps: the 'induced map' included left lateral temporal cortical regions and the hippocampus; the 'spontaneous map' included prefrontal cortical regions and the thalamus. Our combined fMRI/EEG approach allowed to computationally untangle two parallel patterns of alpha modulations and underpin their anatomical basis in the human brain. These findings suggest that the human alpha rhythm represents at least two simultaneously occurring processes which characterize the 'resting brain'; one is related to expected change in sensory information, while the other is endogenous and independent of stimulus change.
Previous research has indicated that the frequency of skin conductance responses without external stimulation or motor activity is a reliable indicator of psychophysiological states and traits. Some authors have suggested that cognitions elicit nonspecific skin conductance responses. These cognitions may resemble the stimuli that evoke a specific skin conductance response. In a within subjects design (n = 31 graduate students) the onset of nonspecific skin conductance responses triggered a signal for the subject to rate cognitions on several indices. These ratings ("absent" to "fully present") were compared with samples in the absence of phasic electrodermal activity. The subjects' current concerns, negative emotion, subjective arousal, and inner speech were rated to be significantly more intense at the time of nonspecific skin conductance responses compared to electrodermal nonresponding periods. Cognitive processes seem to be concomitants of nonspecific skin conductance responses.
While the brain is ruled to a large extent by chemical neurotransmitters, it is also a bioelectric organ. The collective study of Quantitative ElecrtoEncephaloGraphs (QEEG ? the conversion of brainwaves to digital form to allow for comparison between neurologically normative and dysfunctional individuals), Event Related Potentials (ERPs - electrophysiological response to stimulus) and Neurotherapy (the process of actually retraining brain processes to) offers a window into brain physiology and function via computer and statistical analyses of traditional EEG patterns, suggesting innovative approaches to the improvement of attention, anxiety, mood and behavior. The volume provides detailed description of the various EEG rhythms and ERPs, the conventional analytic methods such as spectral analysis, and the emerging method utilizing QEEG and ERPs. This research is then related back to practice and all existing approaches in the field of Neurotherapy - conventional EEG-based neurofeedback, brain-computer interface, transcranial Direct Current Stimulation, and Transcranial Magnetic Stimulation ? are covered in full. Additionally, software for EEG analysis is provided on CD so that the theory can be practically utilized on the spot, and a database of the EEG algorithms described in the book can be combined with algorithms uploaded by the user in order to compare dysfunctional and normative data. While it does not offer the breadth provided by an edited work, this volume does provide a level of depth and detail that a single author can deliver, as well as giving readers insight into the personl theories of one of the preeminent leaders in the field. Features & Benefits: provide a holistic picture of quantitative EEG and event related potentials as a unified scientific field. present a unified description of the methods of quantitative EEG and event related potentials. give a scientifically based overview of existing approaches in the field of neurotherapy provide practical information for the better understanding and treatment of disorders, such as ADHD, Schizophrenia, Addiction, OCD, Depression, and Alzheimer's Disease CD containing software which analyzes EEG patterns and database sample EEGs / Reader can see actual examples of EEG patterns discussed in book and can upload their own library of EEGs for analysis.
Electrodermal activity is one of the most frequently used psychophysiological evaluations in psychology research. Based on the 1992 edition of this work Electrodermal Activity covers advances in the field since the first publication in 1992. The current volume includes updated information on brain imaging techniques such as PET and fMRI, which provide further insight into the brain mechanisms underlying EDA. In addition, this volume is able to describe more reliably hypotheses that have been successfully tested since the first publication. © Springer Science+Business Media, LLC 2012. All rights reserved.
The comorbidity of current and lifetime DSM-IV anxiety and mood disorders was examined in 1,127 outpatients who were assessed with the Anxiety Disorders Interview Schedule for DSM-IV :Lifetime version (ADIS-IV-L). The current and lifetime prevalence of additional Axis I disorders in principal anxiety and mood disorders was found to be 57% and 81%, respectively. The principal diagnostic categories associated with the highest comorbidity rates were mood disorders, posttraumatic stress disorder (PTSD), and generalized anxiety disorder (GAD). A high rate of lifetime comorbidity was found between the anxiety and mood disorders; the lifetime association with mood disorders was particularly strong for PTSD, GAD, obsessive-compulsive disorder, and social phobia. The findings are discussed in regard to their implications for the classification of emotional disorders.
The category “Anxiety Disorders”, as classified in DSM-IV, includes disorders that not only differ phenomenologically but also in their physiologic reactivity to stressor from each other. Patients with episodic anxiety disorders, such as phobic disorder, respond physiologically like non-anxious individuals to everyday demands, except that they overreact to pathology-specific stimuli. Patients with chronic anxiety disorders, such as generalized anxiety disorder, panic disorder, post-traumatic stress disorder and obsessive-compulsive disorder, respond to everyday stressors with less physiologic change than do non-anxious individuals but with strong, often excessive, autonomic responses to pathologyspecific stimuli. This article reviews briefly the peripheral somatic response patterns of anxiety disorders, their communalities and differences in response to everyday stressors and to pathology-specific stressors. Increased muscle tension, a peripheral manifestation of central arousal, is present in all anxiety disorders during stress; however, the contribution of the sympathetic and parasympathetic nervous system to autonomic responses vary considerably. Moreover, manifestations of anxiety are modified by constitutional factors and, when present, aggravated by comorbid physical illnesses.
In this [textbook], Kenneth Hugdahl presents a comprehensive introduction to the history, methods, and applications of psychophysiology and explores other areas concerned with the "mind–body interface," such as psychosomatic medicine, behavioral medicine, clinical psychology, psychiatry, neuropsychology, and cognitive neuroscience. By showing how social, behavioral, cognitive, and emotional events are mirrored in physiological processes, he gives us a clearer understanding of complex cognitive processes.
This book illustrates psychophysiology's importance as a research and clinical tool and highlights its many contributions to the assessment and diagnosis of physical disorders. It also provides a framework for extending psychophysiological insights to other areas of psychology and neuroscience. (PsycINFO Database Record (c) 2012 APA, all rights reserved)
It is argued that the attentional strategies of phobic patients have important consequences for how they cope with anxiety. The literature indicates that focused attention to anxiety cues is important for long-term emotional habituation but that it is made difficult by anxiety. Questionnaire studies of agoraphobics reliably identified factors concerned with attentional strategies of coping with anxiety, and showed that they were distinct from self-talk strategies. The effect of anxiety levels on the use and perceived helpfulness of these strategies was also explored. Finally, the implications of an attentional framework for exposure treatments of phobic anxiety are discussed. It is suggested that the questionnaire may be a useful way of measuring patients' attentional strategies in clinical work.
This article reviews data on the prevalence of panic, social phobia, generalized anxiety, and posttraumatic stress disorder, and research documenting the comorbidity of these disorders with major depression (MDD). These anxiety disorders are frequently comorbid with MDD, and 50–60% of individuals with MDD report a lifetime history of one or more of these anxiety disorders. The anxiety disorders are also highly correlated with one another, and approximately one-quarter to one-half of individuals with each of the anxiety disorders report a lifetime history of an alcohol or substance use disorder. Anxiety disorders rarely exist in isolation, with several studies reporting that over 90% of individuals with anxiety disorders have a lifetime history of other psychiatric problems. Implications for research are discussed, including the potential benefit of using combined categorical and dimensional rating scale approaches in future genetic, biochemical, neuroimaging, and treatment studies. The clinical implications of the findings are also discussed, and the results of recent clinical trials summarized. Available data suggests selective serotonin reuptake inhibitors are the first-line pharmacological treatment for these disorders, and that newer serotonin and norepinephrine reuptake inhibitors show significant promise, especially for comorbid cases. Comorbidity among depression and anxiety disorders is associated with greater symptom severity, and a considerably higher incidence of suicidality. Increased public awareness about these disorders and the availability of effective treatments is sorely needed. Depression and Anxiety, Volume 12, Supplement 1:69–76, 2000. Published 2000 Wiley-Liss, Inc.†
Gray's two‐factor learning theory postulates a behavioral activation system (BAS), a behavioral inhibition system (BIS), and a nonspecific arousal system receiving excitatory inputs from both the BAS and the BIS. The BAS initiates behavior in response to conditioned stimuli for reward (approach) or for relieving nonpunishment (active avoidance). The BIS, which is viewed as an anxiety system, inhibits behavior in response to cues for punishment (passive avoidance) or frustrative nonreward (extinction), and its activity is decreased by the anti‐anxiety drugs (alcohol, barbiturates, minor tranquilizers). Thus, the BIS is an arousal system which inhibits rather than energizes behavior.
A review of the literature suggests that heart rate (HR) is strongly associated with activity of the BAS. This interpretation subsumes the previous findings of cardiac‐somatic coupling, incentive effects on HR, and increased HR in connection with active coping in the face of threat. Electrodermal activity (EDA), on the other hand, increases when there is an activation of the BIS. A consideration of these differing effects on HR and EDA permits a specification of conditions in which these two measures will or will not show directional fractionation.
With this theoretical model it is possible to relate the clinical features of psychopathy to the psychophysiological data with the single assumption that primary psychopaths have a deficient BIS. As a result, they show normal approach, active avoidance, and HR, but they suffer from poor passive avoidance and extinction with reduced EDA in response to threatening stimuli.
A three-stage schema-based information processing model of anxiety is described that involves: (a) the initial registration of a threat stimulus; (b) the activation of a primal threat mode; and (c) the secondary activation of more elaborative and reflective modes of thinking. The defining elements of automatic and strategic processing are discussed with the cognitive bias in anxiety reconceptualized in terms of a mixture of automatic and strategic processing characteristics depending on which stage of the information processing model is under consideration. The goal in the treatment of anxiety is to deactivate the more automatic primal threat mode and to strengthen more constructive reflective modes of thinking. Arguments are presented for the inclusion of verbal mediation as a necessary but not sufficient component in the cognitive and behavioral treatment of anxiety.
In ICD-10 (World Health Organization, 1992) the term agoraphobia refers to an overlapping cluster of phobias. Feared situations include travelling alone, being in crowds or public places and entering shops. Lack of an immediate exit is a key trigger for anxiety, and many sufferers fear collapsing in public.In DSM-IV-TR (American Psychiatric Association, 2000) agoraphobia itself is not a codable disorder, but is defined as follows (see also page 36 for diagnostic criteria).
•Anxiety about being in places or situations from which escape might be difficult (or embarrassing) or help might not be available in the event of having an unexpected or situationally predisposed panic attack or panic-like symptoms. Agoraphobic fears typically involve characteristic clusters of situations that include: being outside the home alone; being in a crowd or standing in a queue; being on a bridge; and travelling in a bus, train or automobile.•The situations are avoided (e.g. travel is restricted) or else are endured with marked distress or with anxiety about having a panic attack or panic-like symptoms, or require the presence of a companion.•The anxiety or phobic avoidance is not better accounted for by another mental disorder.
The cognitive models of panic disorder with (PDA) or without (PD) agoraphobia are now widely recognised. These models propose that patients misinterpret external or internal cues in a catastrophic manner and as a result of these catastrophic cognitions the symptoms are maintained. There is now a large body of empirical evidence for this proposal and the aim of this paper is to systematically review the literature to evaluate whether the empirical evidence supports the contribution of catastrophic cognitions to PD and PDA. Empirical studies using different methodologies, such as interview, questionnaire, self-monitoring, and in vivo techniques are reviewed. The results indicate there is substantial empirical evidence in support of the central role of catastrophic cognition in cognitive models. Different methodologies provided convergent support for the importance of catastrophic cognitions in the maintenance of panic disorder and agoraphobia. Limitations in the interpretation of the existing research are highlighted and future research directions are proposed.
The development of psychotherapy has been based on psychological theories and clinical effects. However, an investigation of the neurobiological mechanisms of psychological interventions is also needed in order to improve indication and prognosis, inform the choice of parallel pharmacotherapy, provide outcome measures and potentially even aid the development of new treatment protocols. This neurobiological investigation can be informed by animal models, for example of learning and conditioning, but will essentially need the non-invasive techniques of functional neuroimaging in order to assess psychotherapy effects on patients' brains, which will be reviewed here. Most research so far has been conducted in obsessive compulsive disorder (OCD), anxiety disorders and depression. Effects in OCD were particularly exciting in that both cognitive behavioural therapy and medication with a selective serotonin inhibitor led to a reduction in blood flow in the caudate nucleus. In phobia, brief courses of behavioural therapy produced marked reductions of paralimbic responses to offensive stimuli in line with the clinical improvement. Findings in depression are less consistent, with both increases and decreases in prefrontal metabolism being reported. However, they are important in pointing to different mechanisms for the clinical effects of pharmacotherapy (more "bottom up") and psychotherapy (more "top down"). For the future it would be desirable if the findings of psychotherapy changes to brain activation patterns were confirmed in larger groups with homogenous imaging protocols. Functional imaging has already made great contributions to the understanding of the neural correlates of psychopathology. For example, evidence converges to suggest that the subgenual cingulate is crucial for mood regulation. One current clinical application of these findings is deep brain stimulation in areas highlighted by such imaging studies. I will discuss their initial application in depression and OCD, and suggest potential alternative options based on recent developments in neurofeedback technology.
Induced alpha power (in a lower, intermediate and upper band) which is deprived from evoked electroencephalograph (EEG) activity was analyzed in an oddball task in which a warning signal (WS) preceded a target or non-target. The lower band, reflecting phasic alertness, desynchronizes only in response to the WS and target. The intermediate band, reflecting expectancy, desynchronizes about 1 s before a target or non-target appears. Upper alpha desynchronizes only after a target is presented and, thus, reflects the performance of the task which was to count the targets. Thus, only slower alpha frequencies reflect attentional demands such as alertness and expectancy.
Panic attacks and the antipanic effect of antidepressants are claimed to distinguish panic disorder (PD) from generalised anxiety disorder. However, most studies showing neurochemical disturbances in PD overlook the non-panic state. We compared panic patients in the non-panic state with controls on biochemical, psychological and physiological measures. There were no differences on the neuroendocrine tests. Self-ratings of bodily and psychological symptoms of anxiety were significantly higher in patients and they scored worse on word recall. Patients had significantly more skin conductance fluctuations and slow wave activity in the electroencephalogram, a sign of hyperventilation which may have implications for brain activity. Discrepancies between patients' self-ratings and objective measures of pulse rate and psychomotor performance indicated that panic patients have distorted perceptions of both physical and mental functioning. Hyperventilation and cognitive distortions in the non-panic state may facilitate panic attacks and are part of the pathophysiology of PD.
Various empirical data suggest that individuals with Panic Disorder (PD) fail to appropriately assign significance to sensory stimuli within the internal and external milieu, including those stimuli which are patently threat-neutral. The failure to appropriately discriminate 'signal' stimuli from among 'noise' signals [Gordon, E., Liddell, B.J., Brown, K.J., Bryant, R., Clark, C.R., Das, P., et al. 2007. Integrating objective gene-brain-behavior markers of psychiatric disorders. J. Integr. Neurosci. 6, 1-34.] results in disturbances of information processing and attentional deployment, which manifests across multiple levels of functioning (e.g., brain, behaviour, autonomic). The present event-related potential (ERP) study, therefore, investigated attentive information processing in PD, using a standard two-tone auditory oddball paradigm, to assess patients' response to infrequent 'target' tones (i.e., signals) and frequent 'non-target' tones (i.e., noise). Simultaneously-recorded autonomic data provided converging measures of the concomitants of disordered information processing. PD patients (n=50) showed increased N1 amplitude to frequent non-target tones and reduced P3 amplitude to infrequent targets, compared to matched controls (n=98). There were no between-group differences for N1 targets, N2 or P2. Patients additionally showed increased heart rate, fewer spontaneous skin conductance responses (trend) to significant stimuli, and reduced P3 latency compared to controls, although the latter result was accounted for by patients who frequently experienced depersonalization and/or derealisation during panic. Patients showed several disturbances of attentive information processing in a simple auditory discrimination task: Increased N1 to repeated stimuli suggests impaired stimulus filtering, whereas reduced P3 amplitude and latency represent the under-allocation of neural resources for infrequent, goal-relevant stimuli, and their increased speed of processing, respectively. These disturbances likely contribute to patients' aversive outcomes in stimulus-rich environments.
Panic disorder is characterized by both specific, phased fear and generalized, chronic anxiety. Standard extinction procedures are efficient in reducing specific fear. However, methods based on human conditioning research - that are capable of reducing chronic anxiety have not yet been thoroughly investigated. This study evaluates a new way of reducing chronic anxiety by signaling aversive events (or by making them more predictable). Using an experimental approach with healthy participants, specific fear and chronic anxiety were operationalized in a within-subjects fear-potentiated startle paradigm by, respectively, conditioning to a cue by presenting predictable shocks and conditioning to a context induced by unpredictable shocks. The results clearly demonstrate that context conditioning is reduced when a discrete cue is added that predicts the onset of the aversive event. The data suggest that making unpredictable events, such as for example panic attacks, predictable, may reduce the generalized and sustained anxiety that often complicates exposure treatment.
It has been demonstrated that patients with panic disorder are more sensitive than normal control subjects to the anxiogenic effects of caffeine. The underlying physiologic basis for this difference is unclear. We examined the electroencephalographic (EEG) activity of seven patients with panic disorder and seven normal control subjects during the randomized double-blind, placebo-controlled administration of oral caffeine (7 mg/kg). EEG data were collected on-line from 28 electrodes; artifact-free epochs were selected manually for off-line Fourier transformation. Caffeine was associated with a significant increase in peak occipital alpha frequency and significant decreases in occipital alpha amplitude, central beta amplitude, and central theta amplitude. Despite the observation that caffeine increased anxiety more in the patients with panic disorder than in the normal control subjects, the two groups did not differ in their EEG responses to caffeine.
The psychological and physiological reactivity of 52 patients with panic disorder to mental arithmetic, cold pressor, and 5% carbon dioxide inhalation tests was compared with that of 26 age- and sex-matched normal subjects. In general, patients with panic disorder were neither more physiologically reactive to these stressors than normal subjects nor slower to recover from them, but they were tonically more anxious and much more likely to ask to stop carbon dioxide inhalation or to report panic attacks during this test. Patients who reported panic attacks (46%) had manifested greater anticipatory anxiety before the gas was delivered, accompanied with increased beta-adrenergic cardiac tone. Thus, anticipatory anxiety can be an important factor in panic provocation. Physiological measures varied greatly in their sensitivity to phasic or tonic anxiety. Carbon dioxide stimulated large increases in respiratory minute volume, but these increases were no greater for patients than for normal subjects.
Skin conductance level (SCL) was measured in 63 subjects with panic disorder, 21 of whom had major depression. Some evidence was found for low SCL being associated with depression, as has been recorded in depression without panic. The standard deviation of SCL was high and it is suggested that the etiology of depression in panic is different from primary depression, at least for some patients. High SCL was not associated with severity of illness. Recordings made in the usual small, isolated, sound-attenuated environment were compared with those made in a larger room with an investigator present for 10 patients and 10 normal controls. Lower SCLs were found in the larger room.
To determine whether panic disorder patients exhibit physiological hyperarousal during rest or during mild, non-panic-inducing stress, 18 patients who experienced frequent panic attacks were compared with nonanxious controls on a battery of physiological assessments. During baseline, patients with panic disorder exhibited higher forehead electromyographic activity, higher systolic blood pressure and higher heart rates than non-anxious volunteers. During psychological stress, heart rate and systolic blood pressure rose more in patients with panic disorder than in nonanxious controls. The skin conductance response, however, was greater and more variable in the nonanxious controls. The results suggest that panic disorder patients with frequent panic attacks exhibit heightened cardiovascular arousal and decreased electrodermal flexibility than nonanxious people, even in nonthreatening situations.
Skin conductance habituation was compared between 38 patients meeting DSM-III criteria for Panic Disorder and 29 normal controls. Approximately half of each group was randomly assigned to be given 100 dB SPL tones and the other half 75 dB tones. All indices pointed to slowed habituation in patients compared with normals: number of trials to response habituation, total number of responses, and slope of decline of skin conductance level. Patient-normal differences were not significantly larger for 100 dB than for 75 dB. In addition, patients compared with normals had more nonspecific fluctuations, higher skin conductance levels, and a shorter response latency to the first stimulus. Stepwise discriminant analyses classified patients and normals better in the 100 dB than in the 75 dB condition, and showed that the various skin conductancy variables were largely redundant at the higher intensity.
1. Quantitative electroencephalographic activity (EEG), together with bioelectric measures of the peripheral nervous system, provide us with unique non-invasive tools for investigating neurobiological issues relating to panic disorder. 2. During recordings of non-panic states, patients with panic disorder exhibit a desynchrony in autonomic vs. somatic arousal levels and also display significant EEG correlations with self-reported anxiety which are not apparent in control subjects. 3. Recordings concomitant with self-reported anxiety/panic during lactate infusions are associated with increased autonomic and somatic arousal and a paradoxical increase in slow wave EEG activity. 4. EEG recordings throughout a lactate challenge indicate that slow wave activity associated with panic does not appear to be characterized by an abrupt, sudden onset but tends to increase gradually throughout the infusion, a finding which is in disaccord with the 'spontaneity' view of panic.
A new off-line procedure for dealing with ocular artifacts in ERP recording is described. The procedure (EMCP) uses EOG and EEG records for individual trials in an experimental session to estimate a propagation factor which describes the relationship between the EOG and EEG traces. The propagation factor is computed after stimulus-linked variability in both traces has been removed. Different propagation factors are computed for blinks and eye movements. Tests are presented which demonstrate the validity and reliability of the procedure. ERPs derived from trials corrected by EMCP are more similar to a 'true' ERP than are ERPs derived from either uncorrected or randomly corrected trials. The procedure also reduces the difference between ERPs which are based on trials with different degrees of EOG variance. Furthermore, variability at each time point, across trials, is reduced following correction. The propagation factor decreases from frontal to parietal electrodes, and is larger for saccades than blinks. It is more consistent within experimental sessions than between sessions. The major advantage of the procedure is that it permits retention of all trials in an ERP experiment, irrespective of ocular artifact. Thus, studies of populations characterized by a high degree of artifact, and those requiring eye movements as part of the experimental task, are made possible. Furthermore, there is no need to require subjects to restrict eye movement activity. In comparison to procedures suggested by others, EMCP also has the advantage that separate correction factors are computed for blinks and movements and that these factors are based on data from the experimental session itself rather than from a separate calibration session.
Describes the development of the Agoraphobic Cognitions Questionnaire and the Body Sensations Questionnaire, companion measures for assessing aspects of fear of fear (panic attacks) in agoraphobics. The instruments were administered to 175 agoraphobics (mean age 37.64 yrs) and 43 controls (mean age 36.13 yrs) who were similar in sex and marital status to experimental Ss. Results show that the instruments were reliable and fared well on tests of discriminant and construct validity. It is concluded that these questionnaires are useful, inexpensive, and easily scored measures for clinical and research applications and fill a need for valid assessment of this dimension of agoraphobia. (22 ref) (PsycINFO Database Record (c) 2012 APA, all rights reserved)
Sympathetic skin nerve action potentials were recorded in the median nerve of 5 healthy college students. A linear and significant correlation was found between the mean voltage amplitude of the sympathetic bursts and the amplitude of skin resistance responses (SRRs). Thus amplitude of skin resistance responses seems to be an index of sympathetic activity.
The psychometric properties of the Depression Anxiety Stress Scales (DASS) were evaluated in a normal sample of N = 717 who were also administered the Beck Depression Inventory (BDI) and the Beck Anxiety Inventory (BAI). The DASS was shown to possess satisfactory psychometric properties, and the factor structure was substantiated both by exploratory and confirmatory factor analysis. In comparison to the BDI and BAI, the DASS scales showed greater separation in factor loadings. The DASS Anxiety scale correlated 0.81 with the BAI, and the DASS Depression scale correlated 0.74 with the BDI. Factor analyses suggested that the BDI differs from the DASS Depression scale primarily in that the BDI includes items such as weight loss, insomnia, somatic preoccupation and irritability, which fail to discriminate between depression and other affective states. The factor structure of the combined BDI and BAI items was virtually identical to that reported by Beck for a sample of diagnosed depressed and anxious patients, supporting the view that these clinical states are more severe expressions of the same states that may be discerned in normals. Implications of the results for the conceptualisation of depression, anxiety and tension/stress are considered, and the utility of the DASS scales in discriminating between these constructs is discussed.