Panic Attacks In Patients Research Articles

Virtual reality exposure therapy for panic disorder

IntroductionVirtual reality exposure therapy (VRET) is a treatment in a virtual environment based on the representation of a patient’s disease in virtual reality. VRET means getting used to a specific situation by intentionally facing the patient’s fearful situation based on the ‘exposure technique.’ By repeatedly exposing the patient to a fearful situation, in the end, inducing the intensity of fear to decrease without avoiding the situation. Virtual reality exposure therapy (VRET) was initially used to treat phobias, anxiety disorders, and stress. It has been proven to be an effective psychotherapy method mainly focusing on acrophobia, flight phobia, arachnophobia, social phobia, and post-traumatic stress disorder (PTSD).ObjectivesVirtual reality exposure therapy (VRET) is used to treat phobias, anxiety disorders, and stress. The virtual reality treatment system can reproduce virtual scenes with the environment modified or removed, and can familiarize patients with such environments. This study aims to verify the degree of improvement of the symptoms of panic disorder by conducting VRET that we have made considering the degree of gradual exposure to the panic disorder group and the control group.MethodsA total of 60 subjects were included in this study, including 43 patients with panic disorder and 17 control group. Subjects were systematically exposed to specific situations over five steps. We checked the heart rate, body temperature, EEG and symptoms before and after exposure using the following assessment instruments; Subjective Units of Discomfort (SUD), Anxiety Sensitivity Index (ASI), Panic Disorder Severity Scale. Repeated measures ANOVA was performed separately for presence, SUDS (distress) scores, and PDSS across time points.ResultsIn the patient group, the program proved to be effective as the sensitivity to anxiety decreased significantly after the VR program (F=3.570, p<0.05). Among the subcategories of ASI, the fear of anxiety symptoms showed statistical significance between sessions (F=3.883, p<0.05) and in the interaction between group and time (F=4.585, p<0.01). The study confirmed the effectiveness of the VR program in situations that mainly induce panic attacks in patients diagnosed with panic disorder (elevator riding, driving a car, driving a car in a tunnel, driving a car in rain). The program effect was significant through repeated measurement ANOVA for each variable of EEG (Alpha, Beta, Delta, Gamma, Theta) (F=3.249, p<0.01).ConclusionsVRET is the process of gradually being exposed to fear stimuli, deliberately confronting and experiencing a fear situation, and learning that nothing dangerous will happen. Even if the patient experiences bodily sensations that are the subject of fear, they can reduce their fear of bodily sensations by repeatedly confirming that they are safe and getting used to them.Disclosure of InterestNone Declared

Clinical case of the coronavirus infection in anamnesis with complication

Abstract: coronavirus infection, the causative agent of which is SARS-CoV-2, can cause a wide range of clinical manifestations. This infection is especially dangerous for patients with a predisposition to cardiovascular diseases, such as hypertension. Changes in vascular tone under conditions of increased blood pressure, as well as dysfunction of vascular walls under the influence of a viral infection, lead to irritation of the suprasegmental part of the autonomic nervous system, namely the posterior part of the hypothalamus, which provokes the development of sympathoadrenal attacks with panic attacks. This study aimed to demonstrate that comorbid disease of the cardiovascular system occurred after coronavirus infection worsens the course of the initial manifestations of cerebrovascular insufficiency. Patient T., who suffered from COVID-19 in October 2020, was examined in the neurological department of the State Institution «Head medical center of the Ministry of Internal Affairs of Ukraine» in December-January 2020-2021. During the examination of the patient’s neurological status, positive pathological reflexes were found: proboscis and Marinescu-Radovichi reflex, foot pathological Strumpell extensor reflex on both sides, and lability of the autonomic nervous system in the form of acrohyperthermia, tremors of the eyelids and fingers of outstretched hands, slight unsteadiness in the Romberg pose. The patient underwent a general blood count, biochemical blood test, Doppler ultrasound of the main arteries of the head, ultrasound of the heart, and electrocardiography (ECG). Special attention should be paid to the results of the Doppler ultrasound of the main arteries of the head: the intima-media complex thickness of the left common carotid artery in the middle third is up to 0.91 mm, in the bifurcation it has a local thickening up to 1.27 mm, the right common carotid artery in the middle third is up to 0.85 mm (normal up to 1.0 mm), in the bifurcation up to 1.04 mm (normal up to 1.1 mm), with partially lost differentiation into layers, echogenicity is not changed. In consequence of the patient’s treatment with statin drugs, scavenger-receptors of monocytes are blocked, the number of which on the surface of cells is stimulated by viruses in the presence of infection, and right to them LDL are attached. Blocking of the capture of LDL by phagocytes limits the formation of foam cells, which are the basis of atherosclerotic plaques, and leads to a decrease in the intima-media complex thickness. According to the results of the ultrasound of the main arteries of the head, after six months of treatment, the thickness of the intima-media complex of the left common carotid artery decreased from 0.91 mm to 0.76 mm, the right one - from 0.85 to 0.65 mm. Conclusions. Comorbid diseases occurring under the influence of coronavirus infection, namely arterial hypertension, worsen the course of such slowly progressive disorders of cerebral blood circulation, as the initial manifestations of cerebral blood circulation insufficiency with the development of sympathoadrenal paroxysms with panic attacks. Treatment with statins, anticoagulants, antihypertensive, nootropic, and sedative drugs helps to stabilize arterial hypertension and reduce the number of sympathoadrenal attacks with panic attacks in patients.

The Degree Centrality and Functional Connectivity in Patients With Temporal Lobe Epilepsy Presenting as Ictal Panic: A Resting State fMRI Study.

ObjectivesIctal panic (IP) can be observed occasionally in patients with temporal lobe epilepsy (TLE). Such descriptions can be found in previous studies, but the mechanism is still not clear and often confused with panic attacks in patients with panic disorder (PD). We try to use imaging methods (resting-state functional magnetic resonance imaging, rs-fMRI) to study the mechanism of this psychiatric comorbidity in patients with TLE.MethodsForty right-onset TLE patients were observed, including 28 patients with TLE but without IP and 12 patients with TLEIP along with 30 gender-age matched healthy controls were included. We collected clinical/physiological/neuropsychological and rs-fMRI data. Degree centrality (DC) and functional connectivity (FC) were calculated. For the DC and FC values, analysis of covariance (ANCOVA) was used to find different areas and t-tests were used to compare differences between the TLEIP, TLE without IP, and healthy control(HC)groups. The relationship between brain abnormalities and patient characteristics was explored by correlation analyses.ResultsNo significant differences in gender and age were found among the three groups, and no significant differences in education level, Montreal Cognitive Assessment (MOCA), Hamilton Depressive Scale (HAMD), Hamilton Anxiety Scale (HAMA), and epilepsy duration (years) between the TLEIP and TLE without IP groups. In addition to fear, other symptoms were observed, including nausea, palpitations, rising epigastric sensation, and dyspnea. There was no correlation between the duration of IP and HAMA. Moreover, all IP durations were <2 min. Compared to the HCs and TLE without IP group, the DC value of the TLEIP group in the left middle temporal gyrus (LMTG) was significantly increased. Compared to the HCs, FC could be found between the LMTG and left inferior temporal gyrus (LITG) in the TLEIP group. In addition, there was FC between the LMTG and cerebellum in the TLEIP group. The difference in the magnitude of FC between the TLEIP vs. HC group was greater than the difference between the TLE vs. HC group.ConclusionsThis study describes brain abnormalities in patients with TLEIP. These results will help to preliminarily understand the mechanism of ictal panic and abnormal functional connection in patients with TLE, and further explore the neuroimaging mechanism of ictal panic in patients with TLE.

Panic Attacks in Patients with Supraventricular Tachycardia: Problems of Differential Diagnosis and Impact on Quality of Life

Aim. To study the psychosomatic relationships and quality of life (QOL) of patients with paroxysmal supraventricular tachycardia (SVT) depending on the presence or absence of panic attacks (PA) in comparison with patients with heartbeat against the background of somatoform autonomic dysfunction.Material and methods. The study included patients with SVT and heart attacks due to sinus tachycardia in the context of somatoform autonomic disorder (SAD). All patients were interviewed to identify anxiety and depressive disorders (Hospital Anxiety and Depression Scale [HADS] and Hamilton's Depression Scale), QOL assessment (SF-36 questionnaire), and they were also consulted by a psychiatrist who established the presence or absence of PA. According to a visual analogue scale, in points from 0 to 6, we assessed the general state of our patients' health (0 points corresponded to complete health, and 6 points corresponded to a serious illness) and the effect of heartbeat on well-being (0 points - no arrhythmia, 6 points - arrhythmia «nterferes with life»).Results. The study included 96 patients: 60 with SVT (21 men, 39 women, average age was 51 [33; 61] years) and 36 with heart attacks caused by sinus tachycardia in the framework of somatoform autonomic disorder (10 men, 26 women, average age was 33 [27; 41] years). Panic disorder was diagnosed in the SVT group in 17 patients, accounting for 28.3%. Only 7 patients (41%) could clearly differentiate between SVT and PA attacks. The low sensitivity of the HADS questionnaire in patients with SVT determined the need to consult a psychiatrist for the diagnosis of panic disorders.Conclusion. PA is typical for 28.3% of patients with SVT. The combination of SVT with PA reduces the QOL of patients due to its mental components, including due to the more frequent occurrence of depressive symptoms. Patients with SAD subjectively perceive the heartbeat as a more significant factor affecting health, compared with patients with SVT. Difficulties in the differential diagnosis of PA and SVT paroxysms in real clinical practice often lead to the appointment of the same therapy without taking into account the differences in the genesis of heartbeats.

A closer look at the relationships between panic attacks, emergency department visits and non-cardiac chest pain.

This study examined the prevalence of emergency department visits prompted by panic attacks in patients with non-cardiac chest pain. A validated structured telephone interview was used to assess panic attacks and their association with the emergency department consultation in 1327 emergency department patients with non-cardiac chest pain. Patients reported at least one panic attack in the past 6 months in 34.5 per cent (95% confidence interval: 32.0%-37.1%) of cases, and 77.1 per cent (95% confidence interval: 73.0%-80.7%) of patients who reported panic attacks had visited the emergency department with non-cardiac chest pain following a panic attack. These results indicate that panic attacks may explain a significant proportion of emergency department visits for non-cardiac chest pain.

Effects of benzodiazepines on anterior cingulate cortex activity during experimentally induced panic

cholecystokinin-tetrapeptide (CCK-4) induces panic symptoms in healthy human subjects, which closely resemble spontaneously occurring panic attacks in patients and provides a safe, valid and reliable experimental model for the investigation of pathophysiological, neurobiological and pharmacological aspects of panic disorder. Benzodiazepines modulate γaminobutyric acid type A (GABAA) receptors throughout the brain. However, it is not fully understood which brain regions within anxiety related brain circuits are really responsible for their anxiolytic effects and how these regions interact. We therefore investigated whether the benzodiazepine alprazolam affects activity in distinct regions within anxiety related brain circuits in humans by means of functional magnetic resonance imaging (fMRI) and experimental induction of panic symptoms with CCK-4.

Clinical and psychophysiological analysis of panic attacksin patients with various mental diseases

The fact that the unilateral approach to studying panic attacks (PA) is unsound has presently become evident in the context of one specialty - neurology or psychiatry. Subjects and methods . One hundred and ninety-three patients with PA, among whom 80 (30 men and 50 women; mean age 31.5±9.66 years) fully met the inclusion-exclusion criteria, were examined. A control group comprised 36 healthy individuals (16 men and 20 women; mean age 25.9±6.73 years). The interdisciplinary approach integrating two (neurological and psychiatric) paradigms was applied to investigate PA. Clinical, psychological, and neurophysiological studies were employed. Results and discussion . The clinical picture of PA and an interattack interval was shown to encompass similar autonomic and different psychopathological manifestations caused by varying pathogenic mechanisms. The clinical manifestations of the latter most frequently correspond to neurotic, specific personality, and schizotypal disorders. It was ascertained that each group of patients with PA, which was identified by the nosological principle, was characterized by the pattern of clinical and psychophysiological characteristics and the trend in PA in addition to general manifestations. The neurophysiological signs of mental disease, in whose picture PA developed, corresponded to the progression of psychopathological and personality manifestations of PA in each consecutive group. The determinant of the pathogenesis and clinical presentation of PA in various mental diseases is psychodynamic processes, the specific features of which need to be taken into account when making diagnostic, therapeutic, prognostic, and expert decisions.

Taking a Family History of Hypertension: Is There Patient Care Benefit?

Taking a Family History of Hypertension: Is There Patient Care Benefit?

Panic attacks simulate presence of somatic illnesses

Panic attacks are characterized with sudden attacks of anxiety with numerous somatic symptoms, such as palpitations, tachycardia, tachypnea, nausea, vertigo. The objective of this study was to analyze symptoms of panic attacks in patients with panic disorder, especially, to determine the specific relationship of somatic and neurological symptoms of panic attacks in boundaries of somatic systems. The study sample consisted of 97 patients with primary diagnosis of panic disorder, without any acute, severe and unstable somatic illness. The presence and frequency of symptoms of panic attacks were estimated by the Panic Disorder Questionnaire. The study results indicate that the most frequent symptoms of panic attacks were cardiological signs (heart pounding or racing) and trembling, followed by unsteady and fainting feeling symptoms, sweating, respiratory symptoms and gastroenterological symptoms. The results of correlation analyses indicate that symptoms of panic attacks classified into cardiovascular, gastro-enterological, respiratory and neurootological systems show statistically significant correlations. The results of analyses of symptoms of panic attacks point to their intercorrelation. This specific association of the symptoms, if they are examined on their own in the patients, could lead to false clinical manifestation of some somatic illness. Therefore, it is necessary to analyze adequately and make the proper differential diagnosis of patients with panic disorder.

Topiramate and Panic Attacks in Patients with Borderline Personality Disorder

Topiramate and Panic Attacks in Patients with Borderline Personality Disorder

Behavioural effects of rapid intravenous administration of meta-chlorophenylpiperazine (m-CPP) in patients with generalized social anxiety disorder, panic disorder and healthy controls

Findings from epidemiological, pharmacotherapeutical, genetic and neurobiological studies suggest a possible overlap in the neurobiology of generalized social anxiety disorder (gSAD) and panic disorder (PD). Previously we have found a rapid intravenous m-CPP challenge of 0.1 mg/kg to be highly sensitive and selective in the provocation of panic attacks in patients with PD. We therefore directly compared the behavioural, neuroendocrine and physiological effects of this rapid m-CPP challenge in a small sample of patients with gSAD, patients with PD and matched healthy controls. Panic attacks were significantly more provoked in patients with PD (85%), but not in patients with gSAD (14%) as compared to healthy controls (0%). Effects on the other behavioural parameters, but not on the neuroendocrine and physiological parameters, were significantly greater in patients with PD compared to patients with gSAD and controls. Our preliminary data do not support a shared neurobiology of gSAD and PD.

Psychopathological profile of 35% CO 2 challenge test–induced panic attacks: a comparison with spontaneous panic attacks

Our aim was to describe the clinical features of 35% CO 2-induced panic attacks in patients with panic disorder (PD) ( Diagnostic and Statistical Manual and Mental Disorders, Fourth Edition) and compare them with the last spontaneous panic attack in patients with PD who had not had a panic attack after the 35% CO 2 challenge test. We examined 91 patients with PD submitted to the CO 2 challenge test. The test consisted of exhaling as fully as possible, took a fast vital capacity breath, held their breath for 8 seconds, exhaled, and then repeated the fast vital capacity breath, again holding for 8 seconds. The patients inhaled the 35% CO 2/65% O 2 mixture or atmospheric compressed air, randomly selected in a double-blind design. Scales were applied before and after the test. A total of 68.1% (n = 62) patients with PD had a panic attack (responders) after the CO 2 test ( χ 2 1 = 25.87, P = .031). The last spontaneous panic attack and the symptom profile from the patients with PD who had not had a panic attack after the test (n = 29, 31.9%) were described to compare. The responders had more respiratory symptoms ( χ 2 1 = 19.21, P < .001), fulfilling the criteria for respiratory PD subtype (80.6%); the disorder started earlier (Mann-Whitney, P < .001), had a higher familial prevalence of PD ( χ 2 1 = 20.45, P = .028), and had more previous depressive episodes ( χ 2 1 = 27.98, P < .001). Our data suggest that there is an association between respiratory PD subtype and hyperreactivity to a CO 2 respiratory challenge test. The responders may be a subgroup of respiratory PD subtype with future diagnostic and therapeutic implications.

Myocardial Perfusion Study of Panic Attacks in Patients With Coronary Artery Disease

Panic disorder (PD) and panic-like anxiety have been associated with an increased risk of cardiovascular death. No study has specifically examined the association between panic attacks and ischemia in patients who have coronary artery disease (CAD). We hypothesized that panic attacks would induce myocardial perfusion defects in patients who have CAD and PD. Sixty-five patients who had CAD and positive results with nuclear exercise stress testing (35 with PD and 30 without PD served as controls) underwent a well-established panic challenge test (1 vital capacity inhalation of a gas mixture containing 35% carbon dioxide and 65% oxygen) and were injected with technetium-99m sestamibi at inhalation. Single-photon emission computed tomography was used to assess per-panic challenge perfusion defects, and heart rate, blood pressure, and 12-lead electrocardiogram were continuously measured during the procedure. Patients were not withdrawn from their cardiac medications. Patients who had PD were significantly younger than the controls; otherwise groups did not differ with respect to gender, cardiac medications, nuclear exercise test results, and baseline heart rate and blood pressure. Seventy-four percent of patients (26 of 35) who had PD had a panic attack at inhalation versus 6.7% of controls (2 of 30, p <0.001). As hypothesized, patients who had PD and demonstrated a panic attack were more likely to develop a reversible myocardial perfusion defect than were controls who did not have an attack (80.9% vs 46.4% p = 0.009). Thus, despite being on their cardiac medications, panic attacks preferentially induced significant perfusion defects in patients who had CAD and PD. In conclusion, panic attacks in patients who have CAD appear to be bad for the heart.

Relationship between anxiety and thyroid function in patients with panic disorder

The aim of this study was to investigate correlations between thyroid function and severity of anxiety or panic attacks in patients with panic disorder. The authors examined 66 out-patients with panic disorder (medicated, n=41; non-medicated, n=25), and measured their free thriiodothyronine (T3), free thyroxine (T4) and thyroid-stimulating hormone (TSH) levels. Significant correlations between the thyroid hormone levels and clinical features were observed in the non-medicated patients. The more severe current panic attacks were, the higher the TSH levels were. In addition, severity of anxiety correlated negatively with free T4 levels. In this study, we discuss relationship between thyroid function and the clinical severity or features of panic disorder.

Effect of Quetiapine in the Treatment of Panic Attacks in Patients with Schizophrenia: 3 Case Reports

The authors describe three schizophrenic patients who suffered from panic attacks and experienced marked improvement of these episodes after switching to quetiapine from their previous antipsychotics (haloperidol, bromperidol, and risperidone), which have high dopamine antagonistic properties such as haloperidol, bromperidol, and risperidone.

Significance of GABAA receptors for the pathophysiology and therapy of panic disorders

Gamma aminobutyric acid (GABA) is the most important inhibitory neurotransmitter in the central nervous system. Its action is exerted in the brain through GABA(A) receptors which belong to the family of ligand-gated ion channels. These GABA(A) receptors consist of various subunits and are targets for benzodiazepines, barbiturates, neuroactive steroids, and distinct anticonvulsive agents. Meanwhile, there is considerable evidence that a dysfunction of GABA(A) receptors plays an important role in the pathophysiology of panic disorder. The anxiolytic effects of benzodiazepines are widely used in the treatment of panic disorder. Nevertheless, side effects of benzodiazepines, e.g., dependency and withdrawal symptoms, limit their use as a long-term treatment. In the meantime, antidepressants, especially selective serotonin reuptake inhibitors, comprise first-line treatment in the pharmacotherapy of panic disorder. They interfere with the synthesis of endogenous neuroactive steroids that allosterically modulate GABA(A) receptor function. With regard to experimentally evoked panic attacks in patients with panic disorder and healthy controls, recent investigations demonstrated that enhancing endogenous GABA through the blockade of the GABA transaminase by vigabatrin or inhibition of GABA transporters by tiagabine may exert anxiolytic effects. This novel strategy targeting the GABA binding site of the GABA(A)/benzodiazepine receptor complex and specific agonists for the benzodiazepine binding site present interesting perspectives for the future pharmacotherapy of panic disorder.

Rodent doxapram model of panic: behavioral effects and c-Fos immunoreactivity in the amygdala

Background Panic attacks, the hallmark of panic disorder, are often characterized by hyperventilation. Existing animal models of anxiety have not addressed the effects of the hyperventilation on anxiety-related behaviors. Doxapram is a respiratory stimulant that reliably evokes panic attacks in patients with panic disorder. We examined doxapram in four rodent models of anxiety and sought to identify brain regions involved in its behavioral effects. Methods The effects of doxapram were determined for cue and contextual fear conditioning, the open field test, and the social interaction test. The effect of doxapram on c-Fos–like immunoreactivity was examined in three brain regions. Results Doxapram at 4 mg/kg increased anxiety-related behaviors in all four anxiety models. An inverted U-shaped dose-response curve was identified for fear conditioning to cue. Doxapram induced c-Fos–like immunoreactivity in the central nucleus of the amygdala but not the lateral nucleus or the nucleus tractus solitarius. Conclusions Doxapram enhanced anxiety-related behaviors in four animal models of anxiety that involve conditioning or spontaneous avoidance. The effect of doxapram may result from activation of neurons in the amygdala. Doxapram, by inducing hyperventilation, may be a useful adjunct to existing animal anxiety models for improving validity for panic anxiety.

A Study of the Phenomenology of Panic Attacks in Patients from India

We studied the symptom structure of panic attacks in 94 patients attending an outpatient psychiatric clinic. Autonomic symptoms of anxiety were reported by the majority of the panic patients. As compared with studies from the West, certain cognitive symptoms, such as fear of loss of control and depersonalization, and vestibular symptoms were endorsed by fewer panic patients. The majority of our panic patients tended to seek help initially from physicians and medical specialists. The majority of the patients also did not experience some DSM-IV symptoms as part of their panic attacks. Comorbid psychiatric conditions influenced the symptom structure of panic attacks. A higher number of agoraphobics as compared with patients with uncomplicated panic disorders had the symptoms of fear of loss of control and fainting. Our findings support the notion that the experience of panic attacks is variable and differs across cultures.

Panic Attacks Associated With Citalopram

Citalopram is the newest selective serotonin reuptake inhibitor (SSRI) available in the United States. It is currently approved by the Food and Drug Administration for the treatment of major depression. However, a number of studies have found it to be effective in the treatment of panic disorder as well. While there have been no previous case reports of citalopram inducing panic attacks in patients, this phenomenon has been reported with other members of the SSRI class of antidepressants. We present the case of a 61-year-old woman who had frank panic attacks after her citalopram dose was increased. She had had no history of anxiety symptoms. Anxiety abated completely upon discontinuance of citalopram therapy.

Panic Attacks Associated With Citalopram

Citalopram is the newest selective serotonin reuptake inhibitor (SSRI) available in the United States. It is currently approved by the Food and Drug Administration for the treatment of major depression. However, a number of studies have found it to be effective in the treatment of panic disorder as well. While there have been no previous case reports of citalopram inducing panic attacks in patients, this phenomenon has been reported with other members of the SSRI class of antidepressants. We present the case of a 61-year-old woman who had frank panic attacks after her citalopram dose was increased. She had had no history of anxiety symptoms. Anxiety abated completely upon discontinuance of citalopram therapy.