The alterations of degree centrality in the frontal lobe of patients with panic disorder.

Objective: The brain network in panic disorder (PD) is still an intriguing issue for research. In this study, we hoped to investigate the role of DC (degree centrality) for the pathophysiology of PD, especially for the fear network. Methods: We enrolled 60 patients with PD and 60 controls in the current study. The gender and age were matched for two groups. All participants received the resting-state functional magnetic resonance imaging to survey the baseline brain activity. Then the DC values of all participants were using REST toolbox. We also compared the DC values between PD and controls. The statistical threshold was set as FDR (false discovery rate) < 0.05. Results: The DC values were significantly lower in the right superior frontal gyrus of PD patients compared to controls (FDR < 0.05). In addition, a negative correlation between the DC values and panic severity was observed in the right superior frontal gyrus and left inferior frontal gyrus. However, there was no significant association between the DC values and illness duration. Conclusion: The DC seemed significantly altered in the frontal lobe of PD patients. The role of the frontal lobe might be more emphasized in the pathophysiology research for PD.

Comparative analysis of default mode networks in major psychiatric disorders using resting-state EEG.

Default mode network (DMN) is a set of functional brain structures coherently activated when individuals are in resting-state. In this study, we constructed multi-frequency band resting-state EEG-based DMN functional network models for major psychiatric disorders to easily compare their pathophysiological characteristics. Phase-locking values (PLVs) were evaluated to quantify functional connectivity; global and nodal clustering coefficients (CCs) were evaluated to quantify global and local connectivity patterns of DMN nodes, respectively. DMNs of patients with post-traumatic stress disorder (PTSD), obsessive compulsive disorder (OCD), panic disorder, major depressive disorder (MDD), bipolar disorder, schizophrenia (SZ), mild cognitive impairment (MCI), and Alzheimer's disease (AD) were constructed relative to their demographically-matched healthy control groups. Overall DMN patterns were then visualized and compared with each other. In global CCs, SZ and AD showed hyper-clustering in the theta band; OCD, MCI, and AD showed hypo-clustering in the low-alpha band; OCD and MDD showed hypo-clustering and hyper-clustering in low-beta, and high-beta bands, respectively. In local CCs, disease-specific patterns were observed. In the PLVs, lowered theta-band functional connectivity between the left lingual gyrus and the left hippocampus was frequently observed. Our comprehensive comparisons suggest EEG-based DMN as a useful vehicle for understanding altered brain networks of major psychiatric disorders.

Could Dispositional Optimism Impair Panic Disorder and Depression Outcomes?

ABSTRACT: The objective of this study was to investigate potential correlates of dispositional optimism and quality of life in patients with depression and panic disorder. The study used a cross-sectional design. The analyzed sample consisted of 77 participants with panic disorder and 75 participants with depression attending two outpatient clinics at the Psychiatry Institute of the Federal University of Rio de Janeiro. Both groups presented similar impairments in optimism and quality of life. In the panic disorder group, optimism scores were significantly correlated with a decrease in anxiety and depression scores (r = 0.26 and r = 0.37, respectively); in the depression group, increases in optimism scores were significantly correlated with decreases in anxiety and depression scores (r = 0.23 and r = 0.3, respectively). The present study showed that high anxiety and depression are correlated with poor optimism and quality of life scores in panic disorder and depression groups. Thus, psychological treatments that can address these topics, besides acute symptoms, are crucial to the absolute recovery of patients.

Vagal control of the heart decreases during increasing imminence of interoceptive threat in patients with panic disorder and agoraphobia.

Theoretically, panic disorder and agoraphobia pathology can be conceptualized as a cascade of dynamically changing defensive responses to threat cues from inside the body. Guided by this trans-diagnostic model we tested the interaction between defensive activation and vagal control as a marker of prefrontal inhibition of subcortical defensive activation. We investigated ultra-short-term changes of vagally controlled high frequency heart rate variability (HRV) during a standardized threat challenge (entrapment) in n = 232 patients with panic disorder and agoraphobia, and its interaction with various indices of defensive activation. We found a strong inverse relationship between HRV and heart rate during threat, which was stronger at the beginning of exposure. Patients with a strong increase in heart rate showed a deactivation of prefrontal vagal control while patients showing less heart rate acceleration showed an increase in vagal control. Moreover, vagal control collapsed in case of imminent threat, i.e., when body symptoms increase and seem to get out of control. In these cases of defensive action patients either fled from the situation or experienced a panic attack. Active avoidance, panic attacks, and increased sympathetic arousal are associated with an inability to maintain vagal control over the heart suggesting that teaching such regulation strategies during exposure treatment might be helpful to keep prefrontal control, particularly during the transition zone from post-encounter to circa strike defense.Trial Registration Number: ISRCTN80046034.

Initial white matter connectivity differences between remitters and non-remitters of patients with panic disorder after 6 months of pharmacotherapy.

Panic disorder (PD) is a harmful mental condition that causes relapsed and persistent impairment. In the treatment of PD, the prognosis for PD should be considered. However, the relationship between pharmacotherapy and biomarkers, for predicting a better response through neuroimaging, is a little known. The purpose of the present study was to examine whether there would be the initial white matter (WM) regions associated with the remission in 6 months. A total of 104 patients with PD were investigated in the study. After six months, there were 17 remission patients with PD and 81 non-remission patients. The Panic Disorder Severity Scale, Albany Panic and Phobia Questionnaire, Anxiety Sensitivity Inventory-Revised, Beck Anxiety Inventory, and Beck Depression Inventory were assessed for all patients at baseline. We compared the diffusion indices between remission and non-remission group at 6 months using Tract-Based Spatial Statistics. The results showed that the fractional anisotropy (FA) values were significantly higher in the non-remitter group compared with those in the remitter group in the WM regions, such as the posterior corona radiata and superior longitudinal fasciculus, at the 6 month evaluation. The logistic regression analysis with clinical symptom severity and FA values of the WM regions as covariates showed that FA values in those regions and the Beck Depression Inventory-II predicted poor remission. This study suggests that posterior corona radiata and superior longitudinal fasciculus are related to potential predictive factors of 6-month remission in patients with PD. WM regions associated with the long-term remission should be verified with further investigations.

Intravenous doxapram administration as a potential model of panic attacks in rats.

Panic disorder can be categorized into the nonrespiratory or the respiratory subtypes, the latter comprising dyspnea, shortness of breath, chest pain, feelings of suffocation, and paresthesias. Doxapram is an analeptic capable of inducing panic attacks with respiratory symptoms in individuals diagnosed with the disorder; however, its neuroanatomical targets and its effects on experimental animals remain uncharacterized. One of the brain regions proposed to trigger panic attacks is the midbrain periaqueductal gray (PAG). Therefore, in this study, we evaluated the effects of doxapram in Fos (c-Fos) protein expression in the PAG and characterized its cardiorespiratory and behavioral effects on the elevated T maze and in the conditioned place aversion (CPA) paradigms. Doxapram increased Fos expression in different columns of the PAG, increased respiratory frequency, decreased heart rate, and increased arterial pressure when injected via intravenous route. Alprazolam, a panicolytic benzodiazepine, injected via intraperitoneal route, decreased respiratory frequency, whereas URB597, an anandamide hydrolysis inhibitor injected via intraperitoneal route, was ineffective. Doxapram injected via intraperitoneal route induced an anxiogenic-like effect in the elevated T-maze model; however, it failed to induce CPA. This study suggests that the cardiorespiratory and behavioral effects of doxapram in rodents serve as an experimental model that can provide insights into the neurobiology of panic attacks.

Psychiatry to dermatology; panic disorder.

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.

Impact of respiratory protective devices on respiration: Implications for panic vulnerability during the COVID-19 pandemic.

BACKGROUND: The wearing of respiratory protective devices (RPDs) correctly and continually in situations where people are at risk of respiratory infections is crucial for infection prevention. Certain people are poorly compliant with RPDs due to RPD-related annoyance, including respiratory discomfort. We hypothesized that individuals vulnerable to panic attacks are included in this group. No published studies on this topic are available. The evidence for our hypothesis was reviewed in this study as a starting point for future research. METHODS: We selected a set of experimental studies that measured the respiratory physiological burden in RPD wearers through objective and validated methods. We conducted a bibliographic search of publications in the PubMed database (January 2000-May 2020) to identify representative studies that may be of interest for panic respiratory pathophysiology. RESULTS: Five studies were included. Wearing RPDs exerted significant respiratory effects, including increased breathing resistance, CO2 rebreathing due to CO2 accumulation in the RPD cavity, and decreased inhaled O2 concentration. We discussed the implications of these effects on the respiratory pathophysiology of panic. LIMITATIONS: Most studies had a small sample size, with a preponderance of young participants. Different methodologies were used across the studies. Furthermore, differences in physical responses between wearing RPDs in experimental settings or daily life cannot be excluded. CONCLUSIONS: This research supports the idea that panic-prone individuals may be at higher risk of respiratory discomfort when wearing RPDs, thereby reducing their tolerance for these devices. Strategies to decrease discomfort should be identified to overcome the risk of poor compliance.

Panic disorder respiratory subtype: psychopathology and challenge tests - an update

Panic disorder (PD) pathophysiology is very heterogeneous, and the discrimination of distinct subtypes could be very useful. A subtype based on respiratory symptoms is known to constitute a specific subgroup. However, evidence to support the respiratory subtype (RS) as a distinct subgroup of PD with a well-defined phenotype remains controversial. Studies have focused on characterization of the RS based on symptoms and response to CO2. In this line, we described clinical and biological aspects focused on symptomatology and CO2 challenge tests in PD RS. The main symptoms that characterize RS are dyspnea (shortness of breath) and a choking sensation. Moreover, patients with the RS tended to be more responsive to CO2 challenge tests, which triggered more panic attacks in this subgroup. Future studies should focus on discriminating respiratory-related clusters and exploring psychophysiological and neuroimaging outcomes in order to provide robust evidence to confirm RS as a distinct subtype of PD.

[Panic and pandemic: Review of the literature on the links between panic disorder and the SARS-CoV-2 epidemic]. / Panique et pandémie : revue de la littérature sur les liens entre le trouble panique et l'épidémie à SARS-CoV-2.

Although the "panic" word has been abundantly linked to the SARS-CoV-2 (severe acute respiratory syndrome coronavirus 2) pandemic in the press, in the scientific literature very few studies have considered whether the current epidemic could predispose to the onset or the aggravation of panic attacks or panic disorder. Indeed, most studies thus far have focused on the risk of increase and aggravation of other psychiatric disorders as a consequence of the SARS-CoV-2 epidemic, such as obsessive-compulsive disorder (OCD), post-traumatic stress disorder (PTSD), and generalized anxiety disorder (GAD). Yet, risk of onset or aggravation of panic disorder, especially the subtype with prominent respiratory symptoms, which is characterized by a fear response conditioning to interoceptive sensations (e.g., respiratory), and hypervigilance to these interoceptive signals, could be expected in the current situation. Indeed, respiratory symptoms, such as coughs and dyspnea, are among the most commonly associated with the SARS-CoV-2 (59-82% and 31-55%, respectively), and respiratory symptoms are associated with a poor illness prognosis. Hence given that some etiological and maintenance factors associated with panic disorder - i.e., fear conditioning to abnormal breathing patterns attributable or not to the COVID-19 (coronavirus disease 2019), as well as hypervigilance towards breathing abnormalities - are supposedly more prevalent, one could expect an increased risk of panic disorder onset or aggravation following the COVID-19 epidemic in people who were affected by the virus, but also those who were not. In people with the comorbidity (i.e., panic disorder or panic attacks and the COVID-19), it is particularly important to be aware of the risk of hypokalemia in specific at-risk situations or prescriptions. For instance, in the case of salbutamol prescription, which might be overly used in patients with anxiety disorders and COVID-19, or in patients presenting with diarrhea and vomiting. Hypokalemia is associated with an increased risk of torsade de pointe, thus caution is required when prescribing specific psychotropic drugs, such as the antidepressants citalopram and escitalopram, which are first-line treatments for panic disorder, but also hydroxyzine, aiming at anxiety reduction. The results reviewed here highlight the importance of considering and further investigating the impact of the current pandemic on the diagnosis and treatment of panic disorder (alone or comorbid with the COVID-19).

In vivo investigation on bio-markers of perimenopausal panic disorder and catgut embedding acupoints mechanism.

BACKGROUND: Panic disorder (PD), defined by repeated and unexpected panic attacks, severely affects patients' living quality and social function. Perimenopausal women are high-risk group of PD and suffer greatly from it. Modern medicine therapies for this disorder have many side reactions and poor effects, so nonpharmacological modality is an urgent need. Although acupoint catgut embedding is widely used in clinical practice, there is no persuasive evidence of its effect for perimenopausal PD. The aim of this study is to investigate the effectiveness and safety of acupoint catgut embedding for perimenopausal PD and to elucidate the correlations among brain neural activation, bio-markers (amino acids) and clinical outcomes with radiographic evidence, thus to explore its neural mechanism. METHODS: The parallel designed, exploratory randomized controlled trial will include 70 outpatients with perimenopausal PD recruited from two hospitals of Chinese Medicine. These subjects will be randomly allocated to an intervention group (Group Embedding) and a control group (Group Medication) in a 1:1 ratio. The subjects in the intervention group will receive acupoint catgut embedding treatment two weeks a time in the following predefined acupuncture points: Shenshu (BL23), Sanyinjiao (SP6), Guanyuan (RN4), Ganshu (BL18), Zusanli (ST36) and Pishu (BL20). The included women of the control group will take 0.4 mg Alprazolam tablet orally, 1 tablet a time, 3 times a day. There is a study period of 3 months and a follow-up period of 1 month for each group. The primary outcomes will be the following therapeutic indexes: the frequency of panic attack, Panic Disorder Severity Score (PDSS), and Panic-associated Symptoms Score (PASS) during the observation period and follow-up period. The changes in Hamilton Anxiety Scale (HAMA) Score and Symptom Checklist 90 (SCL-90) Score will also be compared between these two groups. Additionally, functional magnetic resonance imaging (fMRI) and proton magnetic resonance spectroscopy (1H-MRS) scans will be done before and after the observation period to show cranial neuroimaging changes. DISCUSSION: We present a study design and rationale to explore the effectiveness and neural mechanism of acupoint catgut embedding for perimenopausal PD. There are still several factors restrict our research such as no unified standard of diagnostic criteria and curative effect evaluation. TRIAL REGISTRATION: Chinese Clinical Trial Registry, ChiCTR-INR-16009724, registered in November 2016.

Neural correlates of NOS1 ex1f-VNTR allelic variation in panic disorder and agoraphobia during fear conditioning and extinction in fMRI.

Neuronal nitric oxide synthase (NOS-I) impacts on fear/anxiety-like behavior in animals. In humans, the short (S) allele of a functional promotor polymorphism of NOS1 (NOS1 ex1f-VNTR) has been shown to be associated with higher anxiety and altered fear conditioning in healthy subjects in the amygdala and hippocampus (AMY/HIPP). Here, we explore the role of NOS1 ex1f-VNTR as a pathophysiological correlate of panic disorder and agoraphobia (PD/AG). In a sub-sample of a multicenter cognitive behavioral therapy (CBT) randomized controlled trial in patients with PD/AG (n = 48: S/S-genotype n=15, S/L-genotype n=21, L/L-genotype n=12) and healthy control subjects, HS (n = 34: S/S-genotype n=7, S/L-genotype n=17, L/L-genotype=10), a differential fear conditioning and extinction fMRI-paradigm was used to investigate how NOS1 ex1f-VNTR genotypes are associated with differential neural activation in AMY/HIPP. Prior to CBT, L/L-allele carriers showed higher activation than S/S-allele carriers in AMY/HIPP. A genotype × diagnosis interaction revealed that the S-allele in HS was associated with a pronounced deactivation in AMY/HIPP, while patients showed contrary effects. The interaction of genotype × stimulus type (CS+, conditioned stimulus associated with an aversive stimulus vs. CS-, unassociated) showed effects on differential learning in AMY/HIPP. All effects were predominately found during extinction. Genotype associated effects in patients were not altered after CBT. Low statistical power due to small sample size in each subgroup is a major limitation. However, our findings provide first preliminary evidence for dysfunctional neural fear conditioning/extinction associated with NOS1 ex1f-VNTR genotype in the context of PD/AG, shedding new light on the complex interaction between genetic risk, current psychopathology and treatment-related effects.

Evaluation of TP-E Interval and TP-E/QT Ratio in Panic Disorder.

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.

Movement disorder in a patient with Human Immunodeficiency Virus on an anti-retroviral therapy: A Case Report.

Human Immunodeficiency Virus associated neurocognitive dysfunction can present as a case of movement disorder in a patient with prolonged antiretroviral therapy. Diagnosis was made after ruling out space occupying lesions, nutritional deficiencies and infectious causes through brain imaging and cerebrospinal fluid analysis. With multidisciplinary care and change of antiretroviral therapy to drugs with higher cerebrospinal fluid penetration, symptoms of the patient improved over a span of six months. Delayed neurological damage due to Human Immunodeficiency Virus can present with isolated cerebellar symptoms.

No robust differences in fear conditioning between patients with fear-related disorders and healthy controls.

Fear conditioning and extinction serve as a dominant model for the development and maintenance of pathological anxiety, particularly for phasic fear to specific stimuli or situations. The validity of this model would be supported by differences in the physiological or subjective fear response between patients with fear-related disorders and healthy controls, whereas the model's validity would be questioned by a lack of such differences. We derived pupillometry, skin conductance response and startle electromyography as well as unconditioned stimulus expectancy in a two-day fear acquisition, immediate extinction and recall task and compared an unmedicated group of patients (n = 73) with phobias or panic disorder and a group of patients with posttraumatic stress disorder (PTSD, n = 21) to a group of carefully screened healthy controls (n = 35). Bayesian statistics showed no convincing evidence for a difference in physiological and subjective responses between the groups during fear acquisition, extinction learning or recall. Only the PTSD subgroup had altered startle reactions during extinction learning. Our data do not provide evidence for general differences in associative fear or extinction learning in fear-related pathologies and thereby question the diagnostic validity of the associative fear learning model of these disorders.

Neurocognitive processes in d-cycloserine augmented single-session exposure therapy for anxiety: A randomized placebo-controlled trial.

Drugs targeting N-methyl-d-aspartate (NMDA) receptors and the ability to learn new associations have been proposed as adjunct treatments to boost the success of exposure therapy for anxiety disorders. However, the effects of the NMDA partial agonist d-cycloserine on psychological treatment have been mixed. We investigated potential neurocognitive mechanisms underlying the clinical effects of d-cycloserine-augmented exposure, to inform the optimal combination of this and similar agents with psychological treatment. Panic disorder patients were randomised to single-dose d-cycloserine (250 mg; N = 17) or matching placebo (N = 16) 2hrs before one session of exposure therapy. Neurocognitive markers were assessed one day after treatment, including reaction-time based threat bias for fearful faces (primary outcome) and amygdala response to threat (secondary outcome). Clinical symptom severity was measured the day before and after treatment, and at 1- and 6-months follow-up (secondary outcome). d-cycloserine was associated with greater clinical recovery at 1-month follow-up than placebo (d-cyloserine 71% vs placebo 25%), with the placebo group matching the clinical gains of the d-cycloserine group during 6-months follow-up (d-cycloserine 71% vs placebo 44%). One day after treatment, threat bias for fearful faces and amygdala threat response was lower in the drug compared to placebo group. Lower amygdala magnitude predicted greater clinical improvement during follow-up across groups. While this experimental study is of a preliminary nature due to the limited sample size, these findings highlight a neurocognitive potential mechanism by which d-cycloserine may exert its augmentative effects on psychological treatment and bring forward a marker that may help understand and facilitate development of combination treatments for anxiety. (d-cycloserine Augmented CBT for Panic Disorder; clinicaltrials.gov; NCT01680107).

Further Exploration of Treatment Response in Latinos with Comorbid Asthma and Panic Disorder: A Brief Report of HRV and ETCO2 as Potential Mediators of Treatment Response.

Heart rate variability (HRV) and end tidal CO2 (ETCO2) in relation to treatment response have not been studied in Latino populations or in comorbid asthma and panic disorder (PD). An extension of previously published research, the current study explored psychophysiological variables as possible mediators of treatment response. Latino treatment completers (N = 32) in the Bronx with asthma-PD received either Cognitive-Behavioral Psychophysiological Therapy (CBPT) or Music Relaxation Therapy (MRT). CBPT included HRV-biofeedback (HRVB); in-the-moment heart rate data to help an individual learn to influence his/her own heart rate. The sample was primarily female (93.8%) and Puerto Rican (81.25%). Treatment groups did not differ on demographics, except for less education in CBPT. The Panic Disorder Severity Scale (PDSS) and Asthma Control Questionnaire (ACQ) assessed changes in symptoms. HRV and ETCO2 were measured at four of eight therapy sessions. Baseline ETCO2 and changes in HRV from first to last of psychophysiology sessions were investigated as mediators of change on ACQ and PDSS. Mixed model analyses indicated in the CPBT group, changes in both asthma control and PD severity were not mediated by changes in HRV. In the CBPT and MRT groups combined, changes in PD severity were not mediated by baseline ETCO2. These findings may be due to the brevity of HRVB in CBPT, multiple treatment components, ETCO2 not directly targeted, and/or unique physiological pathways in Latinos with asthma-PD.

Panic disorder respiratory subtype: psychopathology and challenge tests - an update.

Panic disorder (PD) pathophysiology is very heterogeneous, and the discrimination of distinct subtypes could be very useful. A subtype based on respiratory symptoms is known to constitute a specific subgroup. However, evidence to support the respiratory subtype (RS) as a distinct subgroup of PD with a well-defined phenotype remains controversial. Studies have focused on characterization of the RS based on symptoms and response to CO2. In this line, we described clinical and biological aspects focused on symptomatology and CO2 challenge tests in PD RS. The main symptoms that characterize RS are dyspnea (shortness of breath) and a choking sensation. Moreover, patients with the RS tended to be more responsive to CO2 challenge tests, which triggered more panic attacks in this subgroup. Future studies should focus on discriminating respiratory-related clusters and exploring psychophysiological and neuroimaging outcomes in order to provide robust evidence to confirm RS as a distinct subtype of PD.

Treatment-related changes towards normalization of the abnormal external signal processing in panic disorder.

Despite the scientific consensus on the efficacy of psychotherapy for the treatment of psychological disorders, the evidence of treatment-related changes towards normalization of abnormal brain functions in patients is mixed. In the present experiment, we investigated whether treatment can affect early information processing, by testing abnormal event-related potentials (ERPs) evoked by internal and external signals in panic disorder. Sixteen patients with panic disorder and comorbid personality disorder and sixteen control participants performed a response-choice task and a passive viewing task in two testing sessions, separated by around 14 months. During this period, patients received psychological treatment. In agreement with previous studies of performance monitoring, the abnormal amplitude of the Ne/ERN-an index of error processing based on internal signals-did not change between the first and second testing session. However, treatment-related changes were evident for the abnormal vertex positive potential (VPP) evoked by external signals in the response-choice task and the passive viewing task. In patients, the VPP was smaller in the second session compared to the first session, whereas no significant changes occurred in controls. This result supplies evidence of treatment-related changes towards normalization in the early information processing of external visual stimuli in panic disorder.

P50, N100, and P200 Sensory Gating in Panic Disorder.

Panic disorder (PD) has been linked to abnormalities in information processing. However, only little evidence has been published for sensory gating in PD. Sensory gating describes the brain's ability to exclude stimuli of low relevance from higher level information processing, thereby sustaining efficient cognitive processing. Deficits in sensory gating have been associated with various psychiatric conditions, most prominently schizophrenia. In this case-control event-related potential study, we tested 32 patients with PD and 39 healthy controls in a double click paradigm. Both groups were compared with regard to pre-attentive (P50), early-attentive (N100), and late-attentive (P200) sensory gating indices. Contrary to a hypothesized deficit, PD patients and healthy controls showed no differences in P50, N100 and P200 values. These results suggest that sensory gating seems to be functional across the pre-attentive, early-attentive, and late-attentive time span in this clinical population. Given this consistency across auditory sensory gating indices, further research aiming to clarify information processing deficits in PD should focus on other neurophysiological markers to investigate information processing deficits in PD (eg, P300, error-related negativity or mismatch negativity).