Panic Attacks
Dr. Jonathan Haverkampf, M.D.
Panic attacks are sudden periods of intense fear that may include palpitations, sweating, shaking, shortness of breath, numbness, and the ominous feeling that something very bad is going to happen. The maximum degree of symptoms occurs within minutes. There may be a fear of losing control and various somatic symptoms, which induce great anxiety.
Treatment of panic attacks is usually successful and often involves a combination of psychotherapy and medication.
Keywords: panic attack, anxiety, psychotherapy, medication, psychiatry
Contents
Selective Serotonin Reuptake Inhibitors (SSRIs) 6
Introduction
Panic attacks are sudden periods of intense fear that may include palpitations, sweating, shaking, shortness of breath, numbness, and the ominous feeling that something very bad is going to happen. [2] The maximum degree of symptoms occurs within minutes. There may be a fear of losing control or chest pain. [2] The loss of control is usually the cardinal feeling in a panic attack. However, it is the fear of the loss of control which is the problem rather than an actual loss of control.
Panic attacks themselves are usually not dangerous in an otherwise healthy individual. [3] They are distinguished from other forms of anxiety by their intensity and their sudden, episodic nature. [5] They are often experienced in conjunction with anxiety disorders and other psychological conditions, although panic attacks are not generally indicative of a mental disorder.
There are several therapies that work against anxiety with good empirical evidence for their effectiveness such as CBT. Another therapy is communication-focused therapy (CFT), which has been developed by the author to focus directly on the underlying mechanism that many forms of psychotherapy have in common, communication [1].
Often people are not aware of a specific trigger or underlying psychological issues, feelings and emotions that may contribute to a panic attack. An awareness of them usually makes the panic attacks subside and elucidating the underlying dynamics can be an important part of therapy. At the same time, it is important to see the condition in the larger context of how patients engage in communication with themselves and others. Panic attacks and anxiety in general occur because something in the life of the patient is ‘out of sync’. They are an important signal which needs to be taken seriously. Even though panic attacks have a biological component as well, they are more likely to occur if an individual is exposed to a situation which is difficult or conflict rich on the interpersonal level.
Epidemiology
Lifetime prevalence of PAs was 13.2% (SE 0.1%). Among persons that ever had a PA, the majority had recurrent PAs (66.5%; SE 0.5%), while only 12.8% fulfilled DSM‐5 criteria for PD. Recurrent PAs were associated with a subsequent onset of a variety of mental disorders (OR 2.0; 95% CI 1.8–2.2) and their course (OR 1.3; 95% CI 1.2–2.4) whereas single PAs were not (OR 1.1; 95% CI 0.9–1.3 and OR 0.7; 95% CI 0.6–0.8). Cross‐national lifetime prevalence estimates were 1.7% (SE 0.0%) for PD with a median age of onset of 32 (IQR 20–47). Some 80.4% of persons with lifetime PD had a lifetime comorbid mental disorder. We extended previous epidemiological data to a cross‐national context. The presence of recurrent PAs in particular is associated with subsequent onset and course of mental disorders beyond agoraphobia and PD, and might serve as a generic risk marker for psychopathology. (de Jonge et al., 2016)
Co-Morbidity
Panic attacks can occur as part of several mental health conditions, including panic disorder, social anxiety disorder, post-traumatic stress disorder, drug use, depression, and a number of medical problems. [2][4] It is important to rule them out, also to calm the patient, although some patients become even more anxious if they have to undergo medical tests. The best strategy should be decided on an individual level, while not taking unnecessary risks.
Occurrence of DSM-IV panic attacks was strongly related to the subsequent development of various forms of mental disorders—not only panic disorder and agoraphobia. The conditional probability in those with panic attacks to develop other forms of mental disorders was 63% in males and 40% in females. Particularly late onset panic attacks (after the age of 18 years) are associated strongly with the development of multimorbidity of mental disorders. This suggests that panic attacks are generally highly indicative for more severe psychopathology and not only for panic disorder and agoraphobia. (Reed & Wittchen, 1998)
Physicians caring for patients with hypertension should be aware of the significantly greater prevalence of panic attacks in these patients. (Davies et al., 1999)
Panic Attacks are common
In Europe about 3% of the population has a panic attack in a given year while in the United States they affect about 11%. They are more common in females than males. They often begin during puberty or early adulthood. Children and older people are less commonly affected. [2] Panic attacks are, as already mentioned, more frequent when there are changes in life, particularly on a relationship level. While in a good number of cases potential triggers or stressors are not obvious, it always helps to identify what could be potential stressors. As life has become faster and more complex, there is also a greater risk for work related stress.
Symptoms
Panic typically involves an abrupt feeling of catastrophic fear or distress accompanied by physiological symptoms such as palpitations, racing heart, thermal sensations, and sweating. Recurrent unexpected panic attacks (lacking identifiable triggers) and expected panic attacks can also lead to agoraphobia, where subjects with panic disorder avoid situations that were associated with panic attacks. (Johnson et al., 2014) Some people also suffer from tunnel vision, mostly due to blood flow leaving the head to more critical parts of the body in defense. These feelings may provoke a strong urge to escape or flee the place where the attack began (a consequence of the “fight-or-flight response”, in which the hormone causing this response is released in significant amounts). This response floods the body with hormones, particularly epinephrine (adrenaline), which aid it in defending against harm. [5]
Panic attacks can manifest in different forms and have different somatic foci. In one study, five sets of panic symptoms (respiratory, nocturnal, nonfearful, cognitive, and vestibular) have been shown to cluster together at varying degrees of consistency. However, none of these potential subtypes have been shown so far to have any underlying functional differences. (Kircanski et al., 2011)
Mechanism
A panic attack is a response of the sympathetic nervous system (SNS). The most common symptoms include trembling, dyspnea (shortness of breath), heart palpitations, chest pain (or chest tightness), hot flashes, cold flashes, burning sensations (particularly in the facial or neck area), sweating, nausea, dizziness (or slight vertigo), light-headedness, hyperventilation, paresthesia (tingling sensations), sensations of choking or smothering, difficulty moving, and derealization. These physical symptoms are interpreted with alarm in people prone to panic attacks. This results in increased anxiety and forms a positive feedback loop. [6]
Often, the onset of shortness of breath and chest pain are the predominant symptoms. Shallow and rapid breathing can change the pH level in one’s blood, which leads to even more symptoms of a panic attack. To break this vicious cycle is difficult once the panic attack has started. In one study, significant patterns of instability across a number of autonomic and respiratory variables were detected as early as 47 minutes before panic onset. The final minutes before onset were dominated by respiratory changes, with significant decreases in tidal volume followed by abrupt carbon dioxide partial pressure increases. Panic attack onset was characterized by heart rate and tidal volume increases and a drop in carbon dioxide partial pressure. Symptom report was consistent with these changes. Skin conductance levels were generally elevated in the hour before, and during, the attacks. Changes in the matched control periods were largely absent. (Meuret et al., 2011)
From a neuropsychological perspective, panic attacks can be conceptualized as an unconditioned circa defense response pattern to intense internal threat stimuli, characterized by strong autonomic surge and escape behavior and abnormal plastic changes of the brain. Anxious apprehension develops after the experience of such severe panic attacks as conditioned responses to mild body symptoms. Theoretically these conditioned fear responses can be considered as post-encounter defense characterized by increased selective attention, increased threat appraisal and defensive freezing and startle potentiation evidencing altered brain circuits evoked by mild body symptoms. Agoraphobic avoidance starts very early during the defensive cascade and can be conceived as motivated behavior driven by the incentive to be in a safe context that is under control of the individual. (Hamm et al., 2014)
Common risk factors include smoking and psychological stress. Similar symptoms to panic attacks can be caused hyperthyroidism, hyperparathyroidism, heart disease, lung disease, and drug use. [2]
Even during this particular attack, the degree of hyperventilation was not impressive. Findings indicate that the hypothesis that hyperventilation is an important symptom-producing mechanism in panic may be dismissed. (Garssen et al., 1996)
Nocturnal panickers report higher intolerance of uncertainty than daytime panickers, more responsibility for harm than daytime panickers. Nocturnal and daytime panickers report similar AS physical concerns. similar AS cognitive concerns. Nocturnal panickers report higher AS social concerns than daytime panickers. Nocturnal panickers endorsed greater inhibitory intolerance of uncertainty and responsibility for harm, but not prospective intolerance of uncertainty, or anxiety sensitivity physical or cognitive concerns. This study provides support for the fear of loss of vigilance theory and suggests intolerance of uncertainty and responsibility for harm reduction be targeted in treatment for nocturnal panic attacks. (Smith et al., 2019)
The assumption of a generally hyperactive amygdala in PD seems to apply more to state than trait characteristics of PD, and involvement of further areas in the fear circuit, such as anterior cingulate and insula, is suggested. Furthermore, genetic risk variants have been proposed to partly drive fear network activity. Thus, the present state of knowledge generally supports limbic and cortical prefrontal involvement as originally proposed in the neuroanatomical hypothesis. Some modifications might be suggested regarding a potential extension of the fear circuit, genetic factors shaping neural network activity and neuroanatomically informed clinical subtypes of PD potentially guiding future treatment decisions. (Dresler et al., 2013)
Results suggest that heightened sensitivity to threat and reduced sensitivity to reward may be specific components of PD and MDD, respectively. In addition, relative to noncomorbid depression and PD, comorbid MDD and PD may be characterized by heightened NT, but not abnormal levels of these “specific” components. (Shankman et al., 2013)
Both groups exhibited dependence on and were comforted by having an MP; however, people with PD and agoraphobia showed significantly more emotional alterations as well as intense physical and psychological symptoms when they were apart from or unable to use an MP compared to healthy volunteers. (Anna Lucia Spear King et al., 2014)
Besides genetic vulnerability factors, personality and behavioral characteristics, such as anxiety sensitivity, neuroticism, and cognitive appraisal might moderate the influence of life events on the development of panic disorder. (Klauke et al., 2010)
This study demonstrates the link between cerebral correlates of cognitive (IFG) and emotional (“fear network”) processing during symptom improvement across time in PD/A. Further research along this line has promising potential to support the development and further optimization of targeted treatments. (Kircher et al., 2013)
Asmong these, the gene encoding monoamine oxidase A (MAOA) is noteworthy given that genetic variation has been demonstrated to influence gene expression and monoamine levels. Long alleles of the MAOA-uVNTR promoter polymorphism are associated with PD/AG and correspond with increased enzyme activity. Carriers of the risk allele had significantly worse outcome as measured by the Hamilton Anxiety scale (46% responders vs 67%, P=0.017). This was accompanied by elevated heart rate and increased fear during an anxiety-provoking situation, that is, the behavioral avoidance task. All but one panic attack that happened during this task occurred in risk allele carriers and, furthermore, risk allele carriers did not habituate to the situation during repetitive exposure. Finally, functional neuroimaging during a classical fear conditioning paradigm evidenced that the protective allele is associated with increased activation of the anterior cingulate cortex upon presentation of the CS+ during acquisition of fear. Further differentiation between high- and low-risk subjects after treatment was observed in the inferior parietal lobes, suggesting differential brain activation patterns upon CBT. Taken together, we established that a genetic risk factor for PD/AG is associated with worse response to CBT and identify potential underlying neural mechanisms. These findings might govern how psychotherapy can include genetic information to tailor individualized treatment approaches. (Reif et al., 2014)
Overall, panic disorder patients exceeded control participants in startle reflex and heart rate during imagery of standard panic attack scenarios, concordant with more extreme ratings of aversion and emotional arousal. Accounting for the presence of agoraphobia revealed that both panic disorder with and without situational apprehension showed the pronounced heart rate increases during standard panic attack imagery observed for the sample as a whole. In contrast, startle potentiation to aversive imagery was more robust in those without versus with agoraphobia. Reflex diminution was most dramatic in those with the most pervasive agoraphobia, coincident with the most extreme levels of comorbid broad negative affectivity, disorder chronicity, and functional impairment. Principal panic disorder may represent initial, heightened interoceptive fearfulness and concomitant defensive hyperactivity, which through progressive generalization of anticipatory anxiety ultimately transitions to a disorder of pervasive agoraphobic apprehension and avoidance, broad dysphoria, and compromised mobilization for defensive action. (McTeague et al., 2011)
Models of laterality infer distinct aspects of EEG alpha asymmetry in clinical disorders, which has been replicated for over three decades. EEG alpha asymmetry was assessed in the frontocentral region, for resting Eyes Closed and Eyes Open conditions. Schizophrenia was characterized by significantly greater left lateralized alpha power than controls, indicating a deficit in left frontal activity at rest, which may relate to “disconnections” across wider fronto-temporal networks. The depression group showed a trend-level tendency towards the opposite pattern of greater right-lateralized activity than controls. The remaining anxiety and behavioral disorders did not show any significant deviance in alpha asymmetry from the nssormative control group. However, at a non-significant level laterality for these groups was generally consistent with expected directions, suggesting a propensity towards a particular lateralization but still remaining within the normative range. Overall, the results of the current study indicate that EEG alpha asymmetry may show the most clinical utility as a biomarker for schizophrenia and depression in comparison to other clinical disorders. (Gordon et al., 2010)
s
Causes
It has been doubted that panic attacks can come ‘out of the blue’. One study found that significant autonomic irregularities preceded the onset of attacks that were reported as abrupt and unexpected. (Meuret et al., 2011) One also needs to keep in mind that underlying physiological processes can cause panic attacks. The hypothesis that in some patients paroxysmal supraventricular tachycardia is the cause, but not the consequence of a panic attack, is based on observations that catheter ablation was able to cure patients presenting with panic disorders. (Frommeyer et al., 2013) Negative affectivity appears to be a nonspecific risk factor for panic attacks and major depression, whereas anxiety sensitivity appears to be a specific factor that increases the risk for 4-symptom panic attacks in adolescents. (Hayward et al., 2000)
These data provide strong evidence for anxiety sensitivity as a risk factor in the development of panic attacks and other anxiety symptoms. (Schmidt et al., 1997) Importantly, AS was found to predict the incidence of anxiety disorder diagnoses and overall Axis I diagnoses in those with no history of Axis I diagnoses at study entry. These are the first data to provide strong prospective evidence for AS as a risk factor in the development of anxiety disorders. (Schmidt et al., 2006)
In another study, results point to the role of severe illnesses and physical symptoms typical of anxiety in significant others in the history of subjects with panic attacks. (Ehlers, 1993) These experiences during childhood and adolescence may contribute to their belief that physical symptoms are dangerous. In contrast, in the study there was no specificity for panic with respect to the Ss’ own physical symptoms or cold-related symptoms.
Data has been presented that indicates that childhood separation anxiety disorder and adult onset panic attacks share a common genetic diathesis that is not observed for childhood overanxious disorder, strongly supporting the hypothesis of a specific genetic etiologic link between the two phenotypes (Roberson-Nay et al., 2012). Studies have linked a recent history of nonclinical, unexpected panic attacks to a significant degree with PTSD symptom severity. (Marshall-Berenz et al., 2011)
Empirical data suggests a significant and substantial relationship between anxiety sensitivity, inhibitory intolerance of uncertainty, and panic disorder symptoms. In one study, inhibitory intolerance of uncertainty accounted for relatively more variance in avoidance symptoms related to panic disorder than did the fears of physical sensations dimension of AS. (Carleton et al., 2013)
Previous research has demonstrated that patients with generalised anxiety disorder, phobias, and obsessive-compulsive disorder show an attentional bias towards threat cues related to their respective disorders. (Ehlers et al., 1988)
Panic attacks are more severe in Panic Disorder (PD-PA) than Social Anxiety (SAD-PA). PD-PA are associated with trauma, inpatient treatment, and benzodiazepine use. SAD-PA have fewer cognitive symptoms and related clinical correlates. (Brown et al., 2015)
The present data provide novel evidence that smoking is associated with an increased risk of panic attacks and that quitting smoking helps reduce such risk. (Bakhshaie et al., 2016)
Those who suffer from panic attacks often do not seek psychological treatment, citing the inability to receive care during their attacks as a contributing factor. Herein, we introduce a mobile health (mHealth) biofeedback system that enables treatment of panic attacks wherever and whenever they occur and describe the results of an initial feasibility study. We find that only three of nine chronic panic attack sufferers experienced a panic attack during the study, potentially suggesting a preventative placebo effect common to similar pharmacological interventions. Of the four panic attacks observed, subjects noted that the act of using their phone to record their physiology during the attack helped to stop the attack. (McGinnis et al., 2019)
The onset of panic tended to be related to life transitions that interacted with relational issues of emotional commitment as well as with expectations of increased independence or with separation and loss. Dysfunctional attachments in childhood may impair the integration of affective and cognitive information leading to problems with the recognition and expression of affects. Online forums provide fresh avenues for exploring narration of sensitive topics from an inside perspective. (Lundin, 2020)
Only Val158Met polymorphism of the catechol-O-methyltransferase gene has been implicated in susceptibility to PD by several studies in independent samples and confirmed in a recent meta-analysis. However, the specific role of this genetic variation in PD requires additional analysis considering its gender- and ethnicity-dependent effect and putative impact on cognitive functions. (Maron et al., 2010)
The case presented here illustrates the dependence of an individual with panic disorder on his MP. A specific approach for this dependence should be used in some panic disorder patients. (Anna Lucia S. King et al., 2010)
Emotion dysregulation in GAD and PD may be the consequence of PFC hypo-activation during emotion regulation, consistent with insufficient top-down control. The relationship between PFC hypo-activation and functional impairment suggests that the failure to engage PFC during emotion regulation may be part of the critical transition from dispositionally high anxiety to an anxiety disorder. (Manber Ball et al., 2013)
Generalized anxiety disorder (GAD) and panic disorder (PD) are among the most common mental disorders in the United States, and they can negatively impact a patient’s quality of life and disrupt important activities of daily living. Evidence suggests that the rates of missed diagnoses and misdiagnosis of GAD and PD are high, with symptoms often ascribed to physical causes. Diagnosing GAD and PD requires a broad differential and caution to identify confounding variables and comorbid conditions. Screening and monitoring tools can be used to help make the diagnosis and monitor response to therapy. The GAD-7 and the Severity Measure for Panic Disorder are free diagnostic tools. Successful outcomes may require a combination of treatment modalities tailored to the individual patient. Treatment often includes medications such as selective serotonin reuptake inhibitors and/or psychotherapy, both of which are highly effective. Among psychotherapeutic treatments, cognitive behavior therapy has been studied widely and has an extensive evidence base. Benzodiazepines are effective in reducing anxiety symptoms, but their use is limited by risk of abuse and adverse effect profiles. Physical activity can reduce symptoms of GAD and PD. A number of complementary and alternative treatments are often used; however, evidence is limited for most. Several common botanicals and supplements can potentiate serotonin syndrome when used in combination with antidepressants. Medication should be continued for 12 months before tapering to prevent relapse. (Locke et al., 2015)
Evidence suggests that childhood separation anxiety disorder may be associated with a heightened risk for the development of other disorders in adulthood. The authors conducted a meta-analysis to examine the relationship between childhood separation anxiety disorder and future psychopathology. A childhood diagnosis of separation anxiety disorder significantly increases the risk of panic disorder and any anxiety disorder. These results support a developmental psychopathology conceptualization of anxiety disorders. (Kossowsky et al., 2013)
Treatment
Since the symptoms of a panic attack are similar to symptoms of severe physical illnesses, they should always be investigated for somatic sources.
a meta-analysis showed that, after controlling for the methodological quality of the studies and the type of control group, the combination of exposure, relaxation training, and breathing retraining gives the most consistent evidence for treating PD. Other factors that improve the effectiveness of treatments are the inclusion of homework during the intervention and a follow-up program after it has finished. Furthermore, the treatment is more effective when the patients have no comorbid disorders and the shorter the time they have been suffering from the illness. (Sánchez-Meca et al., 2010)
Psychotherapy
Psychotherapy should always be a part of treatment. As mentioned, there are various therapeutic approaches. The important part is to match the right therapy to the right patient.
While individuals can have a genetic predisposition towards anxiety and panic attacks, there are usually some underlying emotions or worries that induce and maintain a phase of more frequent panic attacks. Identifying and working through such issues is largely the domain of psychodynamic (or psychoanalytic) psychotherapy. On the other hand, panic attacks and anxiety in general can also be related to unhelpful thoughts and behaviors, which may be learned, which is the domain of cognitive behavioral therapy (CBT), which has the largest empirical evidence base among all the different therapies. Interpersonal Psychotherapy (IPT) may also be helpful, while communication-focused therapy (CFT) is a therapy developed by the author to address and work with the mechanism that is common to practically all the psychotherapies, communication.
CBT has demonstrated its effectiveness in several settings. It has been shown that a brief, specifically targeted CBT intervention can treat panic attacks in COPD patients and prevent the development and worsening of panic-spectrum psychopathology and anxiety symptoms. (Livermore et al., 2010) Results in another study demonstrated the efficacy of therapist-assisted web-CBT in the treatment of panic symptoms. (Ruwaard et al., 2010)
Psychotherapy usually takes some time to work. There should be a sense that it is helping against the panic attacks within the first two or three sessions. However, for a clear and enduring effect it can take months, or in some cases even longer. This is why medication is a valuable support early on in treatment. It does achieve results quicker and gives patients some breathing space from the panic attacks, which can severely constrain a patient’s life, leading to situations where one can become house or even bed bound.
The results on BSQ and ACQ suggest that the fear of body sensations in most cases was reduced before a change occurred in agoraphobic cognitions. These results indicate that a brief three-session exposure-based treatment may be sufficient for this subgroup of panic patients. (Hall & Lundh, 2019)
Psychotherapy can have a direct biological effect on the underlying causes of panic attacks. Epigenetic signatures such as methylation of the monoamine oxidase A (MAOA) gene have been found to be altered in panic disorder. There is empirical evidence that MAOA hypomethylation is a risk marker for panic attacks. Interestingly, data also suggests that the hypomethylation is at least to some degree reversible following a course of CBT. (Ziegler et al., 2016), illustrating how psychotherapy can treat a mental health condition also from the biological side. As the neuronal network of the brain not only generates new information, it is also influenced in it is structure by the flows of information to which it is exposed (Haverkampf, 1995).
Communication-Focused Therapy, as developed by the author, aims to change flows of information through changes in internal and external communication patterns (Haverkampf, 2010, 2017a, 2018b), and specific techniques for panic attacks have been described (Haverkampf, 2012, 2016, 2017b). The rational underlying this approach is that anxiety usually arises when there is an apparent misalignment of information, such as a basic need or aspiration being in conflict with perceptions of the external world or internal information in the form of emotions, thoughts or otherwise being in conflict with each other. Changes in communication patterns internally and externally with others bring about changes in the flow of meaningful information, which can lower the anxiety and lessen the frequency and intensity of panic attacks (Haverkampf, 2017b). Since external communication patterns are a reflection of internal communication patterns, and vice versa, developing awareness for them and experimenting with change can lead to a more enduring improvement in the clinical symptoms of anxiety and panic attacks.
How information, such as emotional information, is processed has been shown to play a significant role in panic attacks. In a study by Baker and colleagues, three emotional processing dimensions distinguished the panic from the control groups: greater control of emotional experiences (‘smothering’ or ‘bottling up’ emotions), greater awareness of feelings and more difficulties in labelling emotions. The investigators suggest that emotional processing deficits act as a vulnerability factor for developing panic attacks (Baker et al., 2004).
Significant between- and within-therapist variability in adherence and competence were observed. Adherence and competence deteriorated significantly over the course of treatment. Higher patient interpersonal aggression was associated with decrements in both adherence and competence. Neither adherence nor competence predicted subsequent panic severity. Conclusions: Variability and “drift” in adherence and competence can be observed in controlled trials. Training and implementation efforts should involve continued consultation over multiple cases in order to account for relevant patient factors and promote sustainability across sessions and patients. (Boswell et al., 2013)
Inhibition-related activation patterns indicated difficulties of behavioural regulation in emotional context. At treatment termination, panic-related symptoms had improved significantly, and fronto-limbic activation patterns were normalized. Our results indicate that short-term psychodynamic treatment leads to changes in fronto-limbic circuitry not dissimilar to previous findings on cognitive–behavioural treatments. (Beutel et al., 2010)
At baseline, nonresponders exhibited enhanced activation in the right pregenual anterior cingulate cortex, the hippocampus, and the amygdala in response to a safety signal. While this activation pattern partly resolved in nonresponders after CBT, successful treatment was characterized by increased right hippocampal activation when processing stimulus contingencies. Treatment response was associated with an inhibitory functional coupling between the anterior cingulate cortex and the amygdala that did not change over time.
Conclusions
This study identified brain activation patterns associated with treatment response in patients with panic disorder with agoraphobia. Altered safety signal processing and anterior cingulate cortex-amygdala coupling may indicate individual differences among these patients that determine the effectiveness of exposure-based CBT and associated neuroplastic changes. Findings point to brain networks by which successful CBT in this patient population is mediated. (Lueken et al., 2013)
Results: Bivariate latent difference score modeling indicated that, as expected, change in catastrophic misinterpretations predicted subsequent reductions in overall symptom severity, panic attack frequency, distress/apprehension, and avoidance behavior. However, change in the various symptom domains was not typically a significant predictor of later interpretation change (except for the distress/apprehension factor). Conclusions: These results provide considerable support for the cognitive model of panic and speak to the temporal sequence of change processes during therapy. (Teachman et al., 2010)
Exercise
Our results suggest that acute exercise ameliorates reduced BDNF concentrations in panic disorder patients and raise the question whether this is also found after long-term exercise training and if it is related to the therapeutic outcome. (Ströhle et al., 2010)
Medication
Medication can be added to prevent the occurrence of panic attacks for a while. This lowers the anxiety of having another panic attack, which in itself lowers the likelihood of having a panic attack.
First line treatment is usually an antidepressant from the group of serotonin reuptake inhibitors (SSRIs) for the long-term in combination with a benzodiazepine, such as alprazolam (Xanax®) or lorazepam (Temesta®), as a standby once-off medication when a panic attack might be approaching. The disadvantage of the benzodiazepines is that they may take up to an hour to work, do so only for up to a couple of hours and, if they are taken regularly, they can be addictive and lead to tolerance. However, many patients find it useful to carry a tablet of alprazolam, diazepam, or lorazepam with them. This already often lowers the fear of having a panic attack (Haverkampf, 2018a) and helps the cycle of being anxious about becoming anxious. If a patient feels some control over the anxiety, it already helps to stop it from occurring again.
Selective serotonin reuptake inhibitors and venlafaxine are currently considered as first-line agents for patients with panic disorder (PD). However, a systematic comparison of newer antidepressants for the treatment of PD is lacking thus far. Eligible studies focusing on PD patients treated with newer antidepressants were entered in the Cochrane Collaboration Review Manager. Our primary outcome measure was the mean change in panic symptoms from the baseline to the endpoint in patients treated with antidepressants as compared with those treated with placebo. Secondary outcome measures included the mean change in the overall anxiety scores and dropout rates. Sensitivity analyses were also carried out. Fifty studies focusing on 5236 patients were included. The following antidepressants were significantly superior to placebo for PD patients with the following increasing order of effectiveness: citalopram, sertraline, paroxetine, fluoxetine, and venlafaxine for panic symptoms and paroxetine, fluoxetine, fluvoxamine, citalopram, venlafaxine, and mirtazapine for overall anxiety symptoms. Aside from reboxetine and fluvoxamine, all drugs were associated with significantly lower dropout rates as compared with placebo. Several clinical variables moderated clinical outcomes. However, because of some inconsistencies across the studies and limited evidence for some drugs under investigation, further head-to-head comparisons are required. (Andrisano et al., 2013)
Mechanisms of change of cognitive behavior therapy for panic disorder were examined. CBT produced large changes in both self-efficacy and anxiety sensitivity.sssSelf-efficacy and anxiety sensitivity uniquely predicted changes in panic symptoms. Anxiety sensitivity changed early in treatment, whereas self-efficacy changed later. Self-efficacy and anxiety sensitivity appear to be distinct mechanisms of change of CBT. (Gallagher et al., 2013)
Tricyclic Antidepressants
Administered chlomipramine (25–200 mg/day) to 20 patients (23–54 yrs old) who had panic disorder or agoraphobia with panic attacks. After 8 wks of treatment 75% of the patients with each diagnosis were asymptomatic. Results support the claim that chlomipramine is highly effective in preventing recurrence of panic attacks. (Gloger et al., 1981)
Selective Serotonin Reuptake Inhibitors (SSRIs)
Selective serotonin reuptake inhibitors (SSRIs) are in many countries the most widely prescribed antidepressants. However, they do not only help against depression, but also against various forms of anxiety and panic attacks. They do their work by increasing the serotonin levels in certain centers in the brain and also by docking on serotonin receptors, where, depending on the receptor subclass, they can have inhibitory or activating effects. Their effectiveness is in line with observations that serotonin receptors, which are encoded in the genes, and their densities may be altered in patients suffering from depression and anxiety.
An SSRI is taken daily, but it may take a month or even longer to notice an effect. The dose is usually increased gradually to find the minimum dose that achieves the desired effect. Most recommendations specify that a patient should be on them for at least six months, but a year or more is often better to have a more enduring effect once the medication is stopped. SSRIs should in generally not be stopped from one day to the next but tapered off.
SSRIs need to be used with caution with some underlying health problems, including diabetes, epilepsy, kidney disease and others. Some SSRIs can react unpredictably with other medicines, including some over-the-counter painkillers and herbal remedies, such as St John’s wort. Some of the more common side effects are:
- feeling agitated, shaky or anxious
- feeling or being sick
- dizziness
- blurred vision
- low sex drive (reduced libido)
- difficulty achieving orgasm during sex or masturbation
- in men, difficulty obtaining or maintaining an erection (erectile dysfunction)
However, the more common side effects, such as queasiness in the stomach, nausea or headache often only occur in the beginning, if at all, and then go away over a couple of days to two weeks. Also, increasing the medication slowly, and in some cases starting with only a quarter tablet, in many cases helps to avoid these side effects. While the sexual side effects and an increase in appetite, if they occur, tend to be more persistent, there are usually ways to mitigate the problem, either by switching the SSRI or in some cases even by adding on another antidepressant, such as bupropion, a dopamine and norepinephrine reuptake inhibitor. The SSRIs can also have side effects which tend to be rarer but can have severe consequences if they occur. QT prolongation, for example, can be an issue with citalopram and escitalopram, while there is considerable doubt backed up with empirical data that it is a serotonin reuptake inhibitor class effect (Ojero-Senard et al., 2017).
Some of the more common SSRIs include escitalopram (Cipralex®, Lexapro®), sertraline (Zoloft®, Lustral®), citalopram (Cipramil®), paroxetine (Paxil®, Seroxat®), fluoxetine (Prozac®) and fluvoxamine (Faverine®). Since there are differences in the affinity for certain serotonin receptor subclasses and other non-serotonin receptors, their side effect profiles differ, as do the preferences for their use in specific condition, such as depression, OCD, anxiety, eating disorder and others.
Dr Jonathan Haverkampf, M.D. (Vienna) MLA (Harvard) LL.M. psychoanalytic psychotherapy (Zurich) trained in medicine, psychiatry and psychotherapy and works in private practice for psychotherapy, counselling and psychiatric medication in Dublin, Ireland. He is the author of several books and over a hundred articles. Dr Haverkampf has developed Communication-Focused Therapy® and written extensively about it. He also has advanced degrees in management and law. The author can be reached by email at jo****************@gm***.com or on the websites www.jonathanhaverkampf.ie and www.jonathanhaverkampf.com.
References
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