Physiological changes during spontaneous panic attacks

Spontaneous panic attacks occured in three anxious female patients during the course of polygraphic recording in a laboratory situation. The concomitant physiological changes are described. Cardiovascular measures and skin conductance showed parallel effects whereas the electromyogram correlated poorly with the other measures. The panic attacks were self-limiting.     

Psychopathological description of hyperventilation-induced panic attacks: a comparison with spontaneous panic attacks

Our aim was to describe the clinical features of hyperventilation-induced panic attacks (HPA) in panic disorder patients - DSM-IV - and to compare them with their spontaneous panic attacks and with spontaneous panic attacks in panic disorder (PD) patients not sensible to the hyperventilation challenge test. We reexamined 88 previously studied PD patients when they were submitted to a hyperventilation challenge test. They were induced to hyperventilate (30 breaths/min) for 4 min and anxiety scales were applied before and after the test. A total of 51.1% (n = 45) PD patients had a panic attack after hyperventilating - HPA (chi(2) = 13.11, d.f. = 1, p = 0.017). The clinical symptoms of the most severe panic attack were recorded by the HPA patient and by the PD patients not sensible to this test (non-HPA; n = 43, 48.9%) in a diary during a 1-week period and then compared. The HPA group had more respiratory symptoms (chi(2) = 15.26, d.f. = 1, p < 0.001), fulfilling the criteria for the respiratory PD subtype (75.6%), the disorder started later (Mann-Whitney, p < 0.001), had a higher familial prevalence of PD (chi(2) = 19.45, d.f. = 1, p = 0.036), and had more previous depressive episodes (chi(2) = 18.74, d.f. = 1, p < 0.001). The HPA group had similar symptomatology in spontaneous attacks and HPA. The HPA group may be regarded as a subgroup of the respiratory panic disorder subtype with diagnostic and therapeutic implications.     

Psychopathological profile of 35% CO2 challenge test-induced panic attacks: a comparison with spontaneous panic attacks

Our aim was to describe the clinical features of 35% CO2-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% CO2 challenge test. We examined 91 patients with PD submitted to the CO2 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% CO2/65% O2 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 CO2 test (chi2(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 (chi2(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 (chi2(1) = 20.45, P = .028), and had more previous depressive episodes (chi2(1) = 27.98, P < .001). Our data suggest that there is an association between respiratory PD subtype and hyperreactivity to a CO2 respiratory challenge test. The responders may be a subgroup of respiratory PD subtype with future diagnostic and therapeutic implications.     

Neurobiological mechanisms of panic anxiety: biochemical and behavioral correlates of yohimbine-induced panic attacks

The effects of yohimbine, an alpha 2-adrenergic receptor antagonist, on anxiety, blood pressure, heart rate, and plasma levels of the norepinephrine metabolite 3-methoxy-4-hydroxyphenylglycol (MHPG) and cortisol were determined in 20 healthy subjects and 68 patients who had agoraphobia with panic attacks or panic disorder. Yohimbine produced panic attacks meeting DSM-III criteria in 37 patients and one healthy subject. The patients reporting yohimbine-induced panic attacks had significantly larger increases in plasma MHPG, cortisol, systolic blood pressure, and heart rate than the healthy subjects. These findings support the hypothesis relating high noradrenergic neuronal activity to the pathophysiology of panic attacks in a subgroup of panic disorder patients.     

Community correlates of outcomes in subjects with panic attacks.

The purpose of this study was to document the association between community factors and mental health outcomes in subjects with panic attacks. Randomly selected adults from 18 census tracts were screened for the presence of panic attacks. A structured interview was used to assess health care utilization, psychiatric morbidity, quality of life, and sense of control over panic. Community measures were obtained from census data. Regression analyses found that each community measure was associated with at least one outcome even when adjusted for individual socioeconomic status and barriers to access. Research concerning mental health outcomes in subjects with panic attacks should include community-level data.     

Cognitive mediation in the affective component of spontaneous panic attacks

Single inhalations of a 50% carbon dioxide/50% oxygen gas mixture were administered to 16 subjects with spontaneous panic attacks and to 16 social phobics who did not experience such attacks. Half of each diagnostic category was randomly allocated to either a no explanation condition in which minimal instructions on expected outcome were provided, or an explanation condition in which all possible sensations were described and attributed to the effects of the gas. Subjects with panic attacks who were given no explanation reported a greater proportion of catastrophic cognitions, greater panic, and a greater similarity of the overall experience to a naturally-occurring panic attack than those with panic attacks who received a full explanation. In contrast, both groups of social phobics reported similar effects to each other, regardless of the explanation given. The results provide support for cognitive mediation in the “panic” component of spontaneous panic attacks.     

Endocrine and physiological changes during "spontaneous" panic attacks

Eight patients with DSM-III-defined panic attacks were compared to four normal subjects on hormonal and physiological variables measured at six predetermined times through 24 hr and also during nine "spontaneous" attacks. Levels at predetermined times were not different, other than a reduction of urinary unconjugated epinephrine in patients. Plasma prolactin was elevated at the peak of most of the attacks and correlated with attack severity. Plasma cortisol and growth hormone, and heart rate, were elevated during some attacks, and plasma norepinephrine showed small increases. Significant plasma epinephrine and MHPG changes were not observed.     

CCK-4: Psychophysiological conditioning elicits features of spontaneous panic attacks

Introduction

Cholecystokinin-tetrapeptide (CCK-4) is an established model to generate subjective panic anxiety. CCK-4 injection also results in consistent and dose-dependent rise of stress hormones. Effects other than upon subjective panic and stress hormone activity have barely been examined. The purpose of the study was to investigate CCK-4 effects on emotional facial expression and especially on fear relevant facial muscles establishing therewith a more objective method to measure subjective panic anxiety.

Methods

20 healthy male subjects were randomly and double-blindedly assigned in two groups (dose groups), each of which was investigated three times once with placebo and twice with 25 μg or 50 μg CCK-4 respectively. Subjects of each group were randomly assigned in two different balanced orders of investigations: CCK-CCK-Placebo vs. Placebo-CCK-CCK. Facial muscle and hypothalamo-pituitary-adrenocortical (HPA)-axis activity were recorded.

Results

CCK-4 led dose-dependently to an increase of panic anxiety, an activation of fear relevant facial muscles and a rise of stress hormones. Whereas placebo administration before CCK-4 revealed no significant panic and stress response, during placebo following CCK-4 stimulations a psychophysiological conditioning effect could be observed without rise in HPA-axis activity.

Discussion

Our findings indicate the possibility to measure different intensities of panic anxiety and conditioning effects with a facial EMG method. Dissociation of HPA-activity and fear relevant facial muscle activity is in accordance with former results about spontaneous panic attacks.     

Sertraline-induced panic attacks

Sertraline is a selective serotonin reuptake inhibitor that is approved by the U.S. Food and Drug Administration for the treatment of major depression, obsessive-compulsive disorder (in adults and children), and panic disorder. Although numerous studies have found sertraline to be very effective in the treatment of anxiety, there have been few case reports of panic attacks actually being induced by treatment with sertraline. In this article, we present the cases of two patients without any personal or family history of anxiety disorders who developed panic attacks shortly after the initiation of sertraline therapy. We will also review the literature in regard to the development of anxiety symptoms during treatment with the newer antidepressants and discuss the neurochemical basis of these antidepressant-induced panic attacks.     

Duloxetine-related panic attacks

Side-effects arising on the grounds of antidepressant administration pose as a substantial obstacle hindering successful depressive disorder treatment. Side-effects, especially those severe or those manifested through dramatic clinical presentations such as panic attacks, make the treatment far more difficult and shake patients' trust in both the treatment and the treating physician. This case report deals with a patient experiencing a moderately severe depressive episode, who responded to duloxetine treatment administered in the initial dose of 30 mg per day with as many as three panic attacks in two days. Upon duloxetine withdrawal, these panic attacks ceased as well. The patient continued tianeptine and alprazolam treatment during which no significant side-effects had been seen, so that she gradually recovered. Some of the available literature sources have suggested the possibility of duloxetine administration to the end of generalised anxiety disorder and panic attack treatment. However, they are outnumbered by the contributions reporting about duloxetine-related anxiety, aggressiveness and panic attacks. In line with the foregoing, further monitoring of each and every duloxetine-administered patient group needs to be pursued so as to be able to evaluate treatment benefits and weigh them against risks of anxiety or panic attack onset.     

Nocturnal panic attacks

The panic-respiration connection has been presented with increasing evidences in the literature. We report three panic disorder patients with nocturnal panic attacks with prominent respiratory symptoms, the overlapping of the symptoms with the sleep apnea syndrome and a change of the diurnal panic attacks, from spontaneous to situational pattern. The implication of these findings and awareness to the distinct core of the nocturnal panic attacks symptoms may help to differentiate them from sleep disorders and the search for specific treatment.     

Modeling panic attacks

The isomorphism of dorsal periaqueductal gray-evoked defensive behaviors and panic attacks was appraised in the present study. Thresholds of electrically induced immobility, trotting, galloping, jumping, exophthalmus, micturition and defecation were recorded before and after acute injections of anxiolytic, anxiogenic and antidepressant drugs. Antidepressant effects were further assessed 24 h after injections of 7–14- and 21-day treatments. Chronic administration of clomipramine (CLM, 5–10 mg/kg) a clinically effective antipanic drug increased the thresholds of immobility (24%), trotting (138%) galloping (75%), jumping (45%) and micturition (85%). The 21-day treatment with fluoxetine (FLX, 1 mg/kg) virtually abolished galloping without changing the remaining responses. Galloping thresholds were also increased by 5 mg/kg acute injections of CLM (19%) and FLX (25%). In contrast, chronically administered maprotiline (10 mg/kg), a noradrenaline (NE) selective reuptake inhibitor, selectively increased the thresholds of immobility (118%). Diazepam (1.8 mg/kg) and midazolam (MDZ, 2.5 mg/kg) failed in attenuating the somatic defensive responses. Yet, the sedative dose of MDZ (5 mg/kg) attenuated immobility. The panicogenic drug, pentylenetetrazole (50 mg/kg), markedly decreased the thresholds of galloping (−51%) and micturition (−66%). These results suggest that whereas immobility is a NE-mediated attentional response, galloping is the panic-like behavior best candidate.     

Hyperventilation and panic attacks

The role of hyperventilation in the aetiology of panic attacks is still unclear. This paper briefly reviews the role of hyperventilation and abnormal respiration to panic attacks and examines the experimental evidence. Evidence has been found that physiological variables such as paCO2 and pH are involved in the aetiology of panic attacks and panic disorder but the extent and the nature of the involvement of cognitive variables is undetermined. Based on current evidence, there is a need to integrate cognitive variables with the physiological framework proposed by the hyperventilation theory. Until clear experimental evidence is produced about the relationships between cognitive and physiological factors, the applicability of hyperventilation in the aetiology and treatment of panic attacks remains in question.     

Hypoglycemia and panic attacks

Many patients with panic disorder believe hypoglycemia causes their symptoms. Of 10 patients with panic disorder given sodium lactate to induce panic, none had evidence of low blood sugar levels when they began to experience anxiety symptoms.