Panic Attacks and Depression

This article examines the ability of the panic attack–posttraumatic stress disorder (PTSD) model to predict how panic attacks are generated and how panic attacks worsen PTSD. The article does so by determining the validity of the panic attack–PTSD model in respect to one type of panic attack among traumatized Cambodian refugees: orthostatic panic (OP) attacks (i.e. panic attacks generated by moving from lying or sitting to standing). Among Cambodian refugees attending a psychiatric clinic, the authors conducted two studies to explore the validity of the panic attack–PTSD model as applied to OP patients (i.e. patients with at least one episode of OP in the previous month). In Study 1, the panic attack–PTSD model accurately indicated how OP is seemingly generated: among OP patients (N = 58), orthostasis‐associated flashbacks and catastrophic cognitions predicted OP severity beyond a measure of anxious–depressive distress (Symptom Checklist‐90‐R subscales), and OP severity significantly mediated the effect of anxious–depressive distress on Clinician‐Administered PTSD Scale severity. In Study 2, as predicted by the panic attack–PTSD model, OP had a mediational role in respect to the effect of treatment on PTSD severity: among Cambodian refugees with PTSD and comorbid OP who participated in a cognitive behavioural therapy study (N = 56), improvement in PTSD severity was partially mediated by improvement in OP severity.

Panic disorder, which is found in about 1.5 percent of the population at some time in their lives, includes recurrent episodes of sudden, unpredictable, intense fear accompanied by symptoms such as palpitations, chest pain, and faintness. Panic attacks, which do not meet these diagnostic criteria fully, are two to three times more prevalent. Since panic symptoms can mimic those of other medical disorders, patients with these symptoms use medical services frequently. To determine the risk of suicidal ideation and suicide attempts in panic disorder and attacks, we studied a random sample of 18,011 adults drawn from five U.S. communities. Subjects who had panic disorder, as compared with other psychiatric disorders, had more suicidal ideation and suicide attempts, with an adjusted odds ratio for suicide attempts of 2.62 (95 percent confidence interval, 1.83 to 3.74). The odds ratio was 17.99 (95 percent confidence interval, 12.18 to 26.58) when the group with panic disorder was compared with subjects who had no psychiatric disorder. Twenty percent of the subjects with panic disorder and 12 percent of those with panic attacks had made suicide attempts. These results could not be explained by the coexistence of major depression or of alcohol or drug abuse. We conclude that panic disorder and attacks are associated with an increased risk of suicidal ideation and suicide attempts. Physicians working in general medical settings and emergency departments should be alert to this problem.

This was a randomised controlled trial (RCT). Participants were randomised to viewing positive images of dentistry and dental or dentally neutral photographs for 2 min in the waiting area prior to their appointment. Anticipatory anxiety assessed by the Venham Picture Test. A significant difference in anticipatory dental anxiety was found between the two groups (median-positive images, 0; median-neutral images, 3; P<0.001). Anticipatory anxiety was not correlated with age (0.04; P>0.05) and there was no significant difference between male and female participants in their level of anticipatory anxiety (median for males, 0.5; median for females, 1; P>0.05). Viewing positive images of dentistry and dentists results in short-term reductions in anticipatory anxiety in children.

Peritraumatic and persistent panic attacks in acute stress disorder

BackgroundAnxiety symptoms (AS) are exacerbated in healthcare workers (HCWs) during the COVID-19 pandemic. Spirituality is known to protect against AS in the general population and it is a construct that differs from religion. It can be assessed using structured questionnaires. A validated questionnaire disclosed three spirituality dimensions: peace, meaning, and faith. In HCWs we investigated the predictors of chronic anxiety (pre-COVID-19 and during the pandemic) and acute anxiety (only during the pandemic), including spirituality in the model. Then, we verified which spirituality dimensions predicted chronic and acute anxiety. Lastly, we studied group differences between the mean scores of these spirituality dimensions.Material and methodsThe study was carried out in a Brazilian Hospital. HCWs (n = 118) were assessed for spirituality at a single time-point. They were also asked about AS that had started pre-COVID-19 and persisted during the pandemic (chronic anxiety), and AS that had started only during the pandemic (acute anxiety). The subjects without chronic anxiety were subdivided into two other groups: acute anxiety and without chronic and acute anxiety. Forward stepwise logistic regressions were used to find the significant AS predictors. First, the model considered sex, age, religious affiliation, and spirituality. Then, the analysis were performed considering only the three spirituality dimensions. Group means differences in the spirituality dimensions were compared using univariate ANCOVAS followed by T-tests.ResultsSpirituality was the most realible predictor of chronic (OR = 0.818; 95%CI:0.752–0.890; p<0.001) and acute anxiety (OR = 0.727; 95%CI:0.601–0.881; p = 0.001). Peace alone predicted chronic anxiety (OR = 0.619; 95%CI:0.516–0.744; p<0.001) while for acute anxiety both peace (OR:0.517; 95%CI:0.340–0.787; p = 0.002), and faith (OR:0.674; 95%CI:0.509–0.892; p = 0.006) significantly contributed to the model. Faith was significantly higher in subjects without AS.ConclusionHigher spirituality protected against chronic and acute anxiety. Faith and peace spirituality dimensions conferred protection against acute anxiety during the pandemic.

Antidepressants and behavior therapy in agoraphobia and obsessive-compulsive disorders: A commentary

Sir: Mirtazapine is a unique antidepressant that involves both serotonergic and noradrenergic enhancement through blockade of the α2-autoreceptor and α2-heteroreceptor.1 It is also a 5-HT2 blocker, which makes it a potential anxiolytic agent.2 Overall, mirtazapine appears to be a useful agent in patients with depression coexisting with anxiety symptoms.3 The following case describes a patient diagnosed with dysthymia who experienced panic attacks upon increasing her dose of mirtazapine, an effect not previously described. Case report. Ms. A was a 23-year-old married woman diagnosed with dysthymia (DSM-IV). Prior to her presentation she had taken no psychotropic agents. She described an unremarkable medical history and was taking no prescribed medications; did not abuse alcohol; denied the use of any illicit substances, tobacco products, or herbal medications; and drank 1 to 2 cups of coffee per day. Ms. A denied any significant psychosocial stressors or significant family psychiatric history. A review of recent laboratory results included a negative pregnancy test and a complete blood count, serum chemistries, and thyroid-stimulating hormone all within normal limits. Ms. A agreed to a trial of mirtazapine initiated at 15 mg/day for 2 weeks and tolerated the dosage without event. At her follow-up appointment, the mirtazapine dose was increased to 30 mg/day to target her residual depressive symptoms. Within 2 days of the dose increase, Ms. A experienced a panic attack consisting of palpitations, shortness of breath, sweating, nausea, hot flushes, and thoughts of losing her mind. Her husband took her to an emergency room where she was evaluated, prescribed alprazolam 0.5 mg to be taken on an as needed basis, and released. Ms. A had several panic attacks over the next week, and these too were alleviated by taking alprazolam. It was decided to decrease the mirtazapine back to 15 mg/day to see if the increased dose might be responsible for the panic attacks; the panic attacks subsequently stopped. After 1 week, the mirtazapine was increased to 30 mg/day to treat the residual depressive symptoms. Unfortunately, the patient experienced panic attacks 1 day within the dose escalation. A decision was made to change agents, and venlafaxine extended release (XR) was initiated at 37.5 mg/day after a 4-day washout period. The venlafaxine XR was increased to 75 mg/day at 2 weeks and titrated to 150 mg/day after 1 month with no panic attacks. Mirtazapine has been looked at in the treatment of panic disorder in a double-blind study of 27 patients treated with either mirtazapine or fluoxetine.4 Mirtazapine has shown favorable results in 4 open-label studies and a case series.5–9 However, there is a case report of a panic attack that occurred during the discontinuation of mirtazapine.10 The panic attacks were unexpected but could have occurred due to increasing serotonergic transmission that produced a short-lived anxiety similar to that sometimes seen when using serotonin reuptake inhibitors.10 The presented case underscores the need for clinicians to be vigilant for side effects when prescribing antidepressant agents.

Bipolar–panic comorbidity in the general population: prevalence and associated morbidity

Panic attacks are common in chronic obstructive pulmonary disease (COPD), and the prevalence of panic disorder is at least 10 times higher than in the general population. In the current study, we examined resistive load perception in patients with COPD with and without panic attacks. We tested competing hypotheses, based on conflicting results of earlier studies, that those patients with COPD with panic attacks or panic disorder would show either heightened or blunted perception of dyspnea as the magnitude of inspiratory resistive loads increased. We compared 20 patients with COPD with panic attacks or panic disorder, 20 patients without panic, and 20 healthy, age-matched subjects using an inspiratory resistive load-testing protocol. We administered a diagnostic interview for panic attacks and panic disorder. We measured perceived dyspnea in response to increasing inspiratory resistive loads (modified Borg scale) and several respiratory variables. Dyspnea ratings increased linearly for all groups as the size of resistive loads increased. No significant differences were found between groups on the respiratory variables. Patients with COPD with panic attacks or panic disorder rated their level of dyspnea significantly higher than did other subjects. Patients with COPD with panic attacks showed heightened sensitivity to inspiratory loads. The result reinforces the influence of psychological factors on symptom perception in this disease.

Specific binding of tritiated clonidine, an alpha 2-adrenergic receptor agonist, and tritiated yohimbine, an alpha 2-adrenergic receptor antagonist, to platelet membranes was measured in persons with panic attacks or major depression and in normal subjects. Plasma catecholamine levels were measured in patients with panic attacks and in normal subjects. The number of binding sites in patients with panic attacks, as measured with tritiated clonidine, was lower than in depressed persons and was the same as in normal subjects. The number in patients with panic attacks, as measured with tritiated yohimbine, was lower than in either depressives or normal subjects. Catecholamine levels were somewhat higher in patients with panic attacks than in normal subjects. Treatment with imipramine hydrochloride decreased the number of sites, as measured with either ligand, in both patient groups and increased catecholamine levels in patients with panic attacks.

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.

Psychopathology of panic attacks in panic disorder

Back to table of contents Previous article Next article Letter to the EditorFull AccessSibutramine and Panic AttacksKAREN BINKLEY, M.D., F.R.C.P.C., and SANDRA R. KNOWLES, B.SC.PHM., KAREN BINKLEYSearch for more papers by this author, M.D., F.R.C.P.C., and SANDRA R. KNOWLESSearch for more papers by this author, B.SC.PHM., Toronto, Ont., CanadaPublished Online:1 Oct 2002https://doi.org/10.1176/appi.ajp.159.10.1793-aAboutSectionsPDF/EPUB ToolsAdd to favoritesDownload CitationsTrack Citations ShareShare onFacebookTwitterLinked InEmail To the editor: Sibutramine, a nonamphetamine appetite suppressant, is a selective norepinephrine, serotonin, and—to a lesser extent—dopamine reuptake inhibitor (1). There have been previous reports of psychosis (2), depression, mood changes, palpitations, and chest tightness associated with sibutramine, and hypomania has been linked to the combination of sibutramine and citalopram (3). However, to our knowledge, there have been no reported exacerbations of panic attacks. We report on a patient who had a history of panic attacks and experienced a recurrence of panic symptoms shortly after starting sibutramine.Ms. A, a 62-year-old woman, had been diagnosed as having panic attacks during her mid-20s and had been initially treated with anxiolytics. She had been panic-free without treatment since her mid-30s, except for two attacks, both of which had occurred after minor surgical procedures.Ms. A started taking sibutramine, 10 mg/day, for weight loss. After 1½ weeks of taking sibutramine, she had two panic attacks in rapid succession. She discontinued the medication for several days and had no further attacks. She then restarted sibutramine and had another panic attack within approximately 3 days. She again discontinued sibutramine and has been asymptomatic for 5 months. Ms. A declined a third exposure to sibutramine. She was not unduly apprehensive about taking medication, and there were no obvious psychological stressors present at the time.While it is not possible to definitively prove a causal relationship between sibutramine and panic attacks, the temporal relationship of the onset and disappearance of the panic attacks to the initiation and discontinuation of sibutramine is suggestive. With the Naranjo Adverse Drug Reactions Probability Scale (4), a high-probability relationship between sibutramine and the panic attacks was demonstrated in our patient. Although the mechanism for this reaction is unknown, physicians prescribing sibutramine should be aware of this potentially important side effect.

To evaluate different responses in norepinephrine (NE), epinephrine (E), heart rate (HR), electrodermal activity (EDA) and subjective ratings to a ‘neutral’ and a ‘patient‐specific’ stressor we compared nine anxiety patients with three or more panic attacks during the past week, 10 patients with no panic attacks during the past week and 10 controls, at baseline as well as during two stressors: a videotape containing horror scenes and a tape showing a patient having a panic attack. Both patient groups exhibited higher base levels of panicky feelings, anxiety, nervousness, NE and EDA. The panic attack tape proved a stressor that induced significantly more pronounced increases in subjective bodily symptoms, NE, E and EDA in the patients with three or more panic attacks. Our data suggest that patients with frequent panic attacks show higher reactivity to a stimulus that recalls previous experiences of panic attacks.

Respiration and its control mechanisms may represent an important system involved in abnormal anxiety. Our aim was to compare the demographic and clinical features of patients with panic disorder (PD) with agoraphobia (DSM-IV) who had a panic attack after both the 35% carbon dioxide (CO(2)) test and the breath-holding test (CPA group), and compare them with PD patients who did not have a panic attack after both tests (NPA group). We examined 76 patients with PD who were administered a 35% CO(2)test and a breath-holding test within a 1-week interval. Anxiety scales were applied before and after each test. A panic attack was induced in 50 (65.8%) patients during the CO(2)test (chi(2) = 28.44, df = 1, P<.001) and in 40 (52.6%) patients during the breath-holding test (chi(2) = 15.35, df = 1, P = .036). All patients who had a panic attack during the breath-holding test also had a panic attack during the CO(2)test (n = 40; CPA group). Twenty-six (34.2%) patients with PD did not have a panic attack after both respiratory tests (NPA group). The CPA group had more (chi(2) = 21.67, df = 1, P = .011) respiratory PD subtype. In the CPA group, the disorder started earlier (Mann-Whitney, P<.001), had a higher familial prevalence of PD (chi(2) = 18.34, df = 1, P = .028), and had more previous depressive episodes (chi(2) = 23.59, df = 1, P<.001). Our data suggest that there is an association between respiratory PD subtype and the response to respiratory challenge tests: CO(2)and breath-holding. The CPA may be confirmed as a subgroup of respiratory PD subtype.