Understanding and Treating Panic Disorder in Children and Adolescents (a meta analysis)

Understanding and Treating Panic Disorder in Children and AdolescentsPanic Disorder is a common anxiety disorder that affects approximately 5% of the population at any given point in time. Because of Panic Disorder’s high rate of prevalence and its physical manifestations, there is a high economic cost to society resulting from frequent absenteeism, less work productivity, substance abuse as well as recurrent visits to emergency rooms. Recent studies have revealed that Panic Disorder is not restricted to the adult population alone. Children and adolescents are affected by Panic Disorder as well. However, Panic Disorder in children are often misdiagnosed and obscured by other presenting problems such as ADHD. This paper discusses the current understanding of children and adolescents with Panic Disorder, treatment approaches, and their efficacy.


Panic Disorder is part of a spectrum of anxiety disorders that include Generalized Anxiety Disorder (GAD), phobias, Obsessive-Compulsive Disorder (OCD), and Posttraumatic Stress Disorder (PTSD) (American Psychiatric Association, 2000). Panic Disorder is a debilitating psychological and emotional disorder that is marked by a heightened sense of anxiety or panic (Dattilio, 2001; Hanisch, Hantsoo, Freeman, Sullivan & Coyne, 2008). In adults, Panic Disorder is estimated to affect anywhere from 4% (Dattilio) to 5% of the U.S. population (Roy-Byrne, Craske & Stein, 2006). In Europe, it is estimated that the spectrum of anxiety disorders that include Panic Disorder rank as the most prevalent of all mental disorders with an adult incidence of 12% per year (Andlin-Sobocki & Wittchen, 2005). In Hong Kong, the 1-year prevalence rate for Panic Disorder is 3.89% (Lee, Tsang & Kwok, 2005).

In the US, the economic cost of anxiety disorder in 1990 is estimated to be $42.3 billion or $1,542 per sufferer. Of this estimate, Panic Disorder and Posttraumatic Stress Disorder (PTSD) exerted the most toll (Greenberg et al., 1999). Panic Disorder is associated with increased use of health care services including hospitalization, emergency room visits, medical consultations with specialists (Marciniak et al., 2005), and increased absenteeism from the workplace and/or decline in workplace productivity (Greenberg et al.).

Further exacerbating the impact of Panic Disorder to the individual suffering from Panic Disorder and the economy, Panic Disorder can lead to maladaptive behaviors such as cigarette smoking (Zvolensky & Bernstein, 2005), alcoholism (Lotufo-Neto & Gentil, 1994) and drug abuse (Ham, Waters & Oliver, 2005; Roy-Byrne, Craske & Stein, 2006). Paradoxically, while research has found that maladaptive behavior such as cigarette smoking and alcoholism may actually contribute and at times increase the likelihood of Panic Disorder, people with Panic Disorder often do so in an attempt to alleviate symptoms of Panic Disorder or escape recurrence of panic attacks (Abrams et al., 2008; Lotufo-Neto; McLeish, Zvolensky, Bonn-Miller & Bernstein, 2006; Zvolensky).

Given the cost imposed upon by Panic Disorder on the economy (Greenberg et al., 1999), a study of possible early intervention becomes necessary to minimize the impact of Panic Disorder on the sufferer as well as on the economy. While there has been numerous research studies conducted on adults, little significant research has been conducted regarding the prevalence of Panic Disorder on children and adolescents. This paper proposes, therefore, to extrapolate upon research outcomes from studies conducted on the adult population and assess the applicability of known successful interventions to children and adolescents.

Diagnostic Features of Panic Disorder

According to the American Psychiatric Association’s Diagnostic Statistical Manual of Mental Disorders (DSM-IV-TR) (2000), panic attacks are marked by the sudden, and without warning, occurrence of at least four of the following symptoms: (a) shortness of breath or smothering sensation; (b) dizziness, unsteady feelings, or faintness; (c) palpitations or accelerated heart rate; (d) trembling or shaking; (e) sweating; (f) choking; (g) nausea or abdominal distress; (h) depersonalization or derealization – a feeling that the sufferer’s body or environment, respectively, is not real; (i) numbness or tingling sensations; (j) hot flashes or chills; (k) chest pain or discomfort; (l) fear of dying; (m) fear of going crazy or losing self-control. To qualify for a panic attack, the symptoms cannot be attributed by the individual to situational stimuli and that the panic attack must peak within ten minutes.

Panic attacks often are triggered by sudden internal stimuli, e.g., heart pounding, muscle twitching, or hand shaking (Ham et al., 2005). Individuals with Panic Disorder associate these internal physical sensations with over-exaggerated fear of catastrophe such as having a heart attack, going crazy or social embarrassment (Barlow, 1992; Doerfler, Connor, Volungis & Toscano, 2007; Hofmann et al., 2007). At other times, however, the source of panic attack can come from external stimuli such as mild ground vibration. Those with Panic Disorder, like those who over-exaggerate the meaning of internal stimuli, interpret their environmental stimuli catastrophically. Without looking for the source of the ground shaking (possibly trash truck collecting trash), those with Panic Disorder may interpret the event as the beginning of a major earthquake (Hofmann et al.).

People who experience panic attacks feel a sense of extreme danger and doom and experience a strong fight or flight response (Hanisch et al., 2008). The panic attack may be interpreted as sign that the person is dying and that the symptoms are indicative of underlying and undiagnosed physiological problems, the person fears losing his mind or control of his environment (Barlow, 1992).

After the first few occurrences of panic attack, people who eventually develop Panic Disorder begin to have intense worry about the next time an attack will happen (Sainz, 2007; Perugi, Frare & Toni, 2007). Oftentimes, as a result of multiple experiences with panic attacks in certain situations and places, agoraphobia can develop. Agoraphobia is characterized by fear of public places or situations when opportunity to escape would be minimal or unlikely (Perugi et al.). Believing that certain places or situations can trigger panic and avoidance of these places and situations would minimize occurrence of panic attacks, many people who suffer from Panic Disorder and Agoraphobia at times become prisoners in their own homes for long periods of time (Bouton, Mineka & Barlow, 2001; Hanisch et al.). However, it is not uncommon to have Panic Disorder without Agoraphobia.

A manifestation of Panic Disorder that supports the claim that panic attack in individuals with Panic Disorder occurs outside of the individual’s consciousness is the phenomena of nocturnal panic. While the majority of panic attacks occur during the day, nocturnal panic occur at night when the person is asleep (Albert, Maina, Bergesio & Bogetto, 2005; Den Boer, 1997). Nocturnal panic is a typical experience for people suffering from Panic Disorder with 71% reporting nocturnal panic (Albert et al.; Merritt-Davis & Balon, 2003). However, nocturnal panic is not well understood and questions remain whether nocturnal panic, in fact, is a more severe manifestation of Panic Disorder or a disability unique from Panic Disorder with different underlying causes and pathology (Merritt-Davis & Balon, 2003).

Experiencing a panic attack in itself does not qualify a person for the diagnosis of Panic Disorder (Bouton et al., 2001). To be diagnosed with Panic Disorder, a panic attack must be followed by at least a month of recurring concerns of having another attack, fear that the panic may be indicative of underlying physiological problems and/or repercussions of the panic attacks, and changes in behavior as a result of the attacks. (American Psychological Association, 2000.)

Etymology of Panic Disorder – Current Theories

A number of theories have been put forth in an attempt to explain the acquisition and maintenance of Panic Disorder. In the early years, theories focused primarily on the influence of either the individual’s social and environment stressors as opposed to biological determinants (Barlow, 1992). From the social and environmental factors perspective, dysfunction in cognitive processing, sensitivity to anxiety and social conditioning are the most prominent (Bouton et al., 2001; Jacobs & Nadel, 1999; Smitherman, 2005). In recent years, however, the significant development of available scientific tools have helped usher in a number of neurobiological theories explaining the genesis of Panic Disorder (Charney, 2003; Sainz, 2007). Among the researches implicating a neurobiological genesis for Panic Disorder cite the role of the autonomic nervous system (Shioiri et al., 2005), amygdala (Charney, 2003; Kohler, Carran, Bilker, O’Connor & Sperling, 2001), and neurotransmitters in the development of Panic Disorder (Smitherman, 2005).

Psychological Foundation of Panic Disorder

Three of the most studied psychological theories for the development of Panic Disorder are cognitive, sensitivity to anxiety and conditioning (Bouton, Mineka & Barlow, 2001).

Cognitive theory posits that some individuals are more prone to internally focus. In the absence of any external stimuli, an individual experiences panic attack when the individual gives catastrophic interpretation to internal body sensations, e.g., acceleration of the heart rate. The fear of impending doom further exacerbates internal body sensations, such as further acceleration of the heart rate which then may lead to dizziness, shortness of breath, trembling, etc. The experience of a panic attack may then lead a person to become hyper-vigilant of somatic cues in the future (Bouton et al., 2001; Perugi et al., 2007). Furthermore, the level of catastrophic meaning the person associates with the physical symptom(s) correlates with the intensity of the panic attack (Hedley, Hoffart, Dammen, Ekeberg & Friis, 2000).

Known as the “fear of fear” (Schmidt, Lerew & Jackson, 1997), anxiety sensitivity is considered as one of most important underlying psychological factor in the activation of panic attack and development of Panic Disorder (Cox, Taylor, Clara, Roberts & Enns, 2008; Scott, Heimberg & Jack, 2000). Anxiety sensitivity occurs when an individual assigns a cataclysmic meaning to internal body sensations when experiencing distress. Cataclysmic interpretations of somatic symptoms include fear of dying, social embarrassment, or going crazy (Bouton et al., 2001). It has been found that anxiety sensitivity affects people of all ages and children as young as six years old (Taylor, 1998).

At first glance, cognitive theory and anxiety sensitivity appear to be interchangeable: both involve hyper-vigilance to internal bodily sensations and both attribute the bodily sensations as indicative of an impending doom, e.g., the individual is having a heart attack, going crazy, or something is or will go wrong. However, while cognitive theory posits that internal bodily sensations are not caused by external stimuli (Bouton et al., 2001), anxiety sensitivity is triggered by known anxiety-provoking events, e.g., taking a test (Schmidt, Lerew et al., 1997).

Conditioning theory or classical conditioning is one of the earliest theories that attempted to explain the psychopathology of Panic Disorder. Under conditioning theory, Panic Disorder develops when a neutral stimulus (also known as conditioned stimulus (CS)), e.g., event, location, or situation, is associated with physical symptoms or behavior (conditioned response (CR) (Bouton et al., 2001; LeDoux, 2002). Laboratory experiments involving rats have proved that conditioning occur easily and, once pairing has occurred, is permanent (LeDoux, 2002).

Neurobiological Bases of Panic Disorder

While not complete, because of advances in scientific research methodology, tools and equipments using genetics, neuroimaging and neurochemical techniques (Charney, 2003), a greater understanding of the way the brain processes information (Sainz, 2007), its structure and neurochemical composition has emerged providing us with new insight and understanding in the development of Panic Disorder.

One focus of research studies suggest that Panic Disorder develops as a result of the interaction between the hippocampus, which is known to mediate memory, and the limbic system, specifically, the amygdala, which play a role in the mediation of emotions (Allain, Bourin, Reymann, Bentue-Ferrer, Patat, et al., 1999; Charney, 2003; Sainz, 2007; LeDoux, 2002) and an individual’s response to environmental cues (Charney). It is proposed that the hippocampus imprints environmental stimuli which are then paired with emotional response(s) imprinted in the amygdala (Charney; Jacobs & Nadel, 1999; Rivas-Vazquez, 2001; Schroeder & Shinnick-Gallagher, 2005).

The role of the amygdala in modulating emotional response to environmental stimuli is highlighted in two concurrent studies by Adolphs, Tranel & Buchanan (2005). In one study involving 52 normal subjects and 22 subjects with damage to the temporal lobe including the amygdala revealed that subjects with damage to the amygdala exhibited reduced fear recognition. Their concurrent study compared four subjects with damage to the hippocampus and one with damage to the amygdala only. The result showed that subjects with damage to the hippocampus exhibited factual memory impairment while subject with damage to the amygdala exhibited impairment in emotional response.

The implication of the association between the hippocampus and amygdala in encoding factual memory (hippocampus) and emotional memory (amygdala) highlight the interrelationship between environmental influences and plasticity of the brain (Adolphs et al., 2005). This knowledge may be helpful in understanding the role of stressful and traumatic life events in the development of Panic Disorder (Gassner, 2004).

Neurochemicals have also been implicated in the adoption and maintenance of Panic Disorder (Zwanzger & Rupprecht, 2005). Fear and anxiety behavior have been found to be influenced by a number of neurotransmitters that include the peptidergic neurotransmitters, corticotrophin-releasing hormone, neuropeptide Y, substance P, the monoaminergic transmitters, norepinephrine, serotonin and dopamine and the amino acid transmitters, gamma aminobutyric acid (GABA) and glutamate (Charney, 2003; Rosenbaum, 1990; Zwanzger & Rupprecht).

Panic Disorder in Children and Adolescents

Previously, Panic Disorder had been thought of as mainly a disorder that affected only adults with an initial onset occurring usually in early adulthood (Hanisch, Hantsoo & Freeman, 2008). Recent research studies, however, suggest that adolescents and prepubertal children suffer from panic attacks and Panic Disorder as well (e.g., Doerfler et al., 2007; Masi, Favilla, Mucci & Millepiedi, 2000; Ollendick, 1998).

In children and adolescents, Panic Disorder is estimated to affect 10% to 15% of the population (Doerfler et al., 2007). Often, however, Panic Disorder in children and adolescents is misdiagnosed and obscured by co-occurring disorders prevalent in this population such as Separation Anxiety Disorder (SAD), Generalized Anxiety Disorder (GAD), Attention Deficit with and without Hyperactivity Disorder (ADHD), Obssessive Compulsive Disorder (OCD), and Oppositional Defiant Disorder (ODD) (Diler et al., 2004; Doerfler et al.).

Illustrating the existence and prevalence of panic attack and Panic Disorder in this population is a study by Goodwin and Gotlib (2004). In a sample of 1,285 children and adolescents from 9 to 17 years old, Goodwin and Gotlib (2004) found that 43 or 3.3% of the sample with a mean age of 13.4 reported experiencing panic attack. The study also found that of those who had experienced panic attack, the likelihood of comorbid anxiety disorders and affective disorders is increased, a finding supported by Masi et al. (2000).

Masi et al. (2000) studied 220 clinically-referred children and adolescents ranging in age from 7 to 18 with a mean age of 14 years old. They found that of the 220 participants, 23 (10.4%) were diagnosed with Panic Disorder. Of the 23 participants diagnosed with Panic Disorder, all exhibited symptoms of another type of anxiety disorder with 73% manifesting symptoms of Separation Anxiety Disorder, 56% specific phobias, 30% diagnosed with Obsessive Compulsive Disorder, and 43% manifesting symptoms of depression. In this sample of clinically-referred youth, Masi et al. (2000) found that fear of dying and depersonalization-derealization was more prevalent than fear of losing touch with reality. Of interest is that only two of the participants in this study diagnosed with Panic Disorder were under the age of ten.

The finding that Panic Disorder in children is comorbid with another disorder is further illustrated by a second study by Massi et al. (2001) involving 43 outpatients ranging in age from 7 to 18 and with a mean age of 14.9. Of the sample, 25.6% had both Bipolar Disorder and Panic Disorder. Likewise, Diler et al. (2004) found that in their study of 2,025 youths ranging in age from 5 to 21 years old, 42 or 2.2% suffered from Panic Disorder. The mean age of sample with Panic Disorder is 15.3 years old. Of those diagnosed with Panic Disorder, 50% also suffered from Generalized Anxiety Disorder, 21.4% from Separation Anxiety Disorder, 11.9% suffered from agoraphobia, 11.9% from simple phobia, 9.5% suffered from OCD, and 7.1% suffered from social phobia.

Doerfler et al. (2007) studied 280 children and adolescents referred to a pediatric psychopharmacology clinic and found that 35 (13%) had Panic Disorder. This study found that the mean age of onset of Panic Disorder is 9.9 years. Like the studies of Masi et al. (2000) and Masi et al. (2001), the study conducted by Doerfler et al. revealed that Panic Disorder occurred frequently with other internalizing and externalizing disorders finding that except for one child, all participants were diagnosed with two or more disorders. As in other studies discussed (Masi et al., 2000; Masi et al. 2001), none of the children/adolescent diagnosed with Panic Disorder were referred due to Panic Disorder. Of the 35 found to suffer from Panic Disorder, 11 were referred due to ADHD while the others were referred because of mood disorders. Like their adult counterparts, Doerfler et al. found that children and adolescents with Panic Disorder consistently report fear of having another panic attack, concerns about the ramifications of the panic attacks, fear of losing control and/or dying, and 51% made behavioral changes as a result of the panic attack(s).

The attribution for the cause of panic attack, however, is different between children and adolescents. Most prepubertal children’s perception of the causes of panic attacks are often externalized (e.g., blaming heart pounding to stress from taking a test) (Doerfler et al., 2007). On the other hand, like adults, adolescents often internalize the causes of their panic attacks. Like adults with Panic Disorder, adolescents tend to give catastrophic meaning to internal cues (e.g., the adolescent believing that he/she may be going crazy because he/she had been at the same spot, well prepared, well rested, has taken so many tests before, yet his/her heart is still pounding uncontrollably) (Doerfler et al., 2007).

The most prevalent physical manifestations of panic attack in children often include heart pounding and beating rapidly, shortness of breath, weakness, light headedness, and perspiration (Doerfler et al., 2007; Masi et al., 2000). Adolescents with Panic Disorder report having chest pains, feeling shaky and loosing balance, and headaches (Masi et al.).

Intervention and Treatment of Panic Disorder

While there is growing body of research studying the segment of the children and adolescent population affected by Panic Disorder, treatment approaches for this population are lacking. There is an abundance of studies, however, exploring the efficacy of various intervention and treatment methods in adults with Panic Disorder using various approaches of cognitive and behavior therapy (CBT) (e.g., Barlow, 1992; Botella et al., 2007; Vincelli, Choi, Molinari, Wiederhold & Riva, 2000) psychopharmacology (e.g., Amore, Magnani, Cerisoli & Ferrari, 1999; Bakker, van Balkom & Spinhoven, 2002), or a combination of both Cognitive Behavior Therapy and psychopharmacology (Mitte, 2005; Schmidt & Smith 2005; Smits, O’Cleirigh & Otto, 2006). At present, treatment approaches for children suffering from Panic Disorder have to be extrapolated from studies that have been conducted on their adult counterparts.

Cognitive Behavior Therapy in the treatment of Panic Disorder

Numerous clinical studies have found Cognitive Behavior Therapy as an effective tool in helping those with Panic Disorder (e.g. Clum, Clum & Surls, 1993; McDermott, 2004; Mitte, 2005; Smits, et al., 2006). Cognitive Behavior Therapy’s effectiveness lies in the assumption that changing and restructuring the irrational beliefs and misinterpretation that individuals diagnosed with Panic Disorder attribute to internal and/or external stimuli will lead to minimization or, at best, extinction of thought processes that lead to panic attacks (Hanisch et al., 2008; Hofmann et al., 2007).

Cognitive Behavior Therapy for Panic Disorder include relaxation and breathing techniques, imagery and in vivo exposure (IVE), virtual reality exposure (VRE), and cognitive restructuring in guiding clients to replace panic-provoking misinterpretation of internal and external stimuli with thoughts that are more reality based (Hofmann et al., 2007; Perugi et al., 2007).

Examples of Cognitive Behavior Therapy intervention using relaxation and breathing techniques for individuals with Panic Disorder include: (a) controlled breathing wherein the person experiencing a panic attack is taught to breath through the nose normally rather than the mouth; (b) slowing the breathing or inhaling through the nose and exhaling through the mouth (Taylor, 2001); and (c) symptom induction and de-escalation wherein the person who experiences panic attacks is induced into experiencing a panic attack in a safe environment by taking short successive breaths. Once a panic attack is imminent, the client is asked about their thought processes, is taught breathing techniques to control panic, and helped to restructure misinterpretation of panic-inducing symptoms (Datillo, 2001).

IVE takes the client to the actual environment or setting and exposes the client to what triggered the panic attacks in a process known as “flooding.” While IVE has been proven to be very effective, the number of those diagnosed with Panic Disorder who seek IVE as a form of treatment for Panic Disorder is low at an estimated 15%-20% (Garcia-Palacios, Hoffman, Kwong See, Tsai & Botella, 2001). The lack of willingness to try IVE can be attributed to the client’s aversion to the feared object and/or environment (Garcia-Palacios et al., 2001). The limitations of IVE is further exacerbated by the amount of time required for therapy, thus its cost, as well as the potential threat to the client’s confidentiality given that such immersion procedures occur in public places (Botella et al., 2007).

To address the problems inherent in IVE, current research has focused on using technology to assess its effectiveness in delivering the feared environment or setting through virtual reality exposure (VRE) (Botella et al., 2007). Through VRE, the client is exposed to a three dimensional, computer-generated panic-inducing situation, environment or setting (Garcia-Palacios et al., 2001). Since VRE is conducted in the safety of the clinician’s office, it is cost effective, requires less time commitment, and is confidential. Furthermore, the virtual scenarios presented can be manipulated depending upon the need of the client with high accuracy (Botella et al., 2004; Vincelli et al., 2000).

The attractiveness of VRE was revealed in two surveys of college students suffering from phobia (Garcia-Palacios et al., 2001). Garcia-Palacios et al. (2001) found that 81% and 89% of each respective group of students preferred VRE over IVE. Garcia-Palacios et al. suggested that curiosity may play a role in the willingness of panic/phobia student-sufferers to try VRE, but points out that by placing treatment in a safe environment, the stigma of receiving treatment is removed.

Cognitive Behavior Therapy is found to be effective in the long term follow-ups of six to nine years (Kenardy, Robinson & Dob, 2005). A study conducted by Kenardy et al. on 89 patients with Panic Disorder found that at six months after treatment, between 63% to 67% of the patients were panic-free. Reassessing 28 of the same patients 6-8 years after treatment, Kenardy et al. found that 57.1% were panic-free.

Psychopharmacology in the treatment of Panic Disorder

The first line of pharmacological treatment for Panic Disorder is benzodiazepines and antidepressants that include selective serotonin reuptake inhibitors (SSRIs), tricyclic antidepressants, and monoamine oxidase (MAO) inhibitors (Beamish, Granello & Belcastro, 2002; Bowden, 1992).

In acute stages of Panic Disorder and when fast relief is required, the group of benzodiazepine medications has been found to be efficacious (Bowden, 1992). The most commonly prescribed in the alleviation of Panic Disorder symptoms are alprazolam (Xanax) and clonazepam (Klonopin) (Beamish, 2002). However, high rate of tolerance, impaired short-term memory, sedation, loss of control of body movement, and withdrawal symptoms when benzodiazepine is discontinued are known side effects (Beamish et al., 2002; Bowden, 1992).

Selective serotonin reuptake inhibitors (SSRIs) are antidepressants that work to decrease the reactivity of serotonin receptors in the brain. By blocking the reabsorption of serotonin back into the synapse, available serotonin is increased in the presynaptic region (Rivas-Vazquez, 2001). It has been found that newer selective serotonin reuptake inhibitors (SSRIs) fluoxetine (Prozac) and fluvoxamine (Luvox) are safer in overdose (Beamish et al., 2002). However, restlessness, insomnia, rash, central nervous system stimulation, headache, sedation, impaired memory, weight loss, impaired motor performance, anxiety, seizures, tremor, excessive perspiration, nausea, vomiting, abdominal pain, diarrhea, sexual dysfunction, and precipitation of mania are all possible side effects (Beamish et al., 2002).

Another group of antidepressants that is commonly used for treatment of Panic Disorder is Tricyclic antidepressants or TCAs. These medications have been shown to reduce the severity of symptoms during panic attacks, decrease the number of panic attacks and have contributed to clients’ overall quality of life (Bakker, van Balkom & Spinhoven, 2002). However, Bakker et al., in their meta-analysis of 43 studies found that while selective serotonin reuptake inhibitors (SSRIs) and tricyclic antidepressants (TCAs) are equally effective in treating Panic Disorder, there are more drop outs with those using tricyclic antidepressants (TCAs) (31%) as opposed to those who were treated with selective serotonin reuptake inhibitors (SSRIs) (18%). Bakker et al. concluded from this study that clients tolerate selective serotonin reuptake inhibitors (SSRIs) better than tricyclic antidepressants (TCAs).

Despite the seeming effectiveness of antidepressants in alleviating the symptoms of panic attacks and Panic Disorder, Charney (2003) concluded that the cause of their effectiveness remains inconclusive. According to Charney, this is true for the role the physiology of the brain plays in the adaptation and maintenance of Panic Disorder as well.

Combining Cognitive Behavior Therapy and Pharmacotherapy in the Treatment of Panic Disorder

If Cognitive Behavior Therapy alone is effective in helping people with Panic Disorder and pharmacotherapy in and of itself has been shown to be effective as well, the question arises whether combining both psychotherapy and pharmacology would yield a better, faster and longer lasting result. The results are inconclusive, at best.

Research studies have shown that while combining pharmacotherapy and Cognitive Behavior Therapy is efficacious in the acute stage of panic attacks, the result reverses when medication is discontinued (Smits, et al., 2006). In fact, the gains of combined treatment with Cognitive Behavior Therapy and medication fades when medication is discontinued. Furthermore, their longitudinal study show that the long term effect is less when compared to Cognitive Behavior Therapy alone (Smits et al.).

To compare the efficacy of Cognitive Behavior Therapy versus medication with Cognitive Behavior Therapy treatment for Panic Disorder, Schmidt and Smith (2005) conducted a study on 178 subjects suffering from Panic Disorder. Of the subjects, 60% received medication of either antidepressant or anxiolytics. Schmidt and Smith (2005) found that the effects of combining Cognitive Behavior Therapy with medication is minimal compared to the effects of Cognitive Behavior Therapy alone in the treatment of Panic Disorder. Furthermore, the study found that while treating patients with higher dosage of benzodiazepine contributed little to the treatment, treating patients with antidepressants resulted in poorer outcome.

Van Apeldoorn, et al. (2008) studied 150 individuals with Panic Disorder. The study compared the efficacy of Cognitive Behavior Therapy alone, SSRI alone against Cognitive Behavior Therapy plus SSRI. Their findings show that Cognitive Behavior Therapy plus SSRI is more effective in treating Panic Disorder than with Cognitive Behavior Therapy or SSRI alone. Van Apeldoorn point out, however, the risk of relapse is high after medication is tapered off. Thus, suggesting that medication alone would be less effective than Cognitive Behavior Therapy alone in the long term.

With current research showing efficacy of Cognitive Behavior Therapy alone and medication alone equal at best, the question turns to financial consideration. In Australia, Heuzenroeder et al. (2004) studied the economic impact of treating Panic Disorder with Cognitive Behavior Therapy or medication. Their cost versus efficacy analysis revealed that, at least in Australia, Cognitive Behavior Therapy intervention is more cost-effective than pharmacological treatment with efficacy being equal.


As we gain better understanding of the underlying causes, the acquisition and maintenance of Panic Disorder, we begin to realize that each psychological and biological theory may have their own merits. Yet, as our knowledge grow, a bigger picture emerges and a greater understanding that maybe each theory is not mutually exclusive and that Panic Disorder may be a result of interplay between all of the theories (Rosenbaum, 1990). While one theory may explain the basis for the acquisition of Panic Disorder for one individual, that same theory may not explain the same phenomena for another individual (see Jacobs & Nadel, 1999). Cognition or learning has been associated with Panic Disorder as evidenced by cases of Panic Disorder involving trauma (see Sainz, 2007; Leskin & Sheikh, 2002;), while the amygdala and hippocampus (see Allain et al., 1999; Charney, 2003; Sainz, 2007; LeDoux, 2002) as well as neurotransmitters (Charney, 2003; Rosenbaum, 1990; Zwanzger & Rupprecht, 2005) have been shown to mediate learning and emotion that are necessary for Panic Disorder. Of further consideration is family transmission of Panic Disorder. In support, research have shown a higher percentage of Panic Disorder characteristics in people with family members suffering from Panic Disorder (Zvolensky & Raulin, 1999).

There is evidence that Cognitive Behavior Therapy by itself through the use of relaxation and breathing techniques, imagery and IVE, VRE, and cognitive restructuring are efficacious in mediating the irrational thought processes of patients with Panic Disorder. The restructured processes give patients more control over the way they interpret and react to both external and internal stimuli. (e.g., Hanisch et al., 2008; Hofmann et al., 2007).

There is also some evidence pointing to the efficacy of pharmacological treatment in the form of antidepressants selective serotonin reuptake inhibitors (SSRIs) and tricyclic antidepressants (TCAs) treating patients with Panic Disorder (Bakker et al., 2002). However, the success of combining both Cognitive Behavior Therapy and pharmacological treatments is inconclusive. Some studies have shown that combining both is most effective (e.g., Dattilio, 2001) while other studies suggest that one counteracts the other and as soon as the patient is weaned from antidepressants, the effect of Cognitive Behavior Therapy fades as well (Schmidt & Smith, 2005; Smits et al., 2006). Schmidt and Smith (2005) suggested that when Panic Disorder patients first present for treatment, it would be prudent to start treatment with Cognitive Behavior Therapy prior to considering combining Cognitive Behavior Therapy with medication.

There are a number of promising leads to the treatment of Panic Disorder. In Cognitive Behavior Therapy, the use of new and evolving technology to create simulation(s) of real life situations is seen as less aversive than IVE and, therefore, more easily accepted by those with Panic Disorder (Botella et al., 2007; Garcia-Palacios et al., 2001; Vincelli et al., 2000). Likewise, there are a number of promising leads in the field of neurophysiology and neurochemistry. Knowledge is growing related to the role different parts of the brain and neurotransmitters play in the acquirement and retention of maladaptive response system that leads to panic attacks and eventually Panic Disorder (Charney, 2003; Ham et al., 2005; Hanisch et al., 2008). Further analysis of current research in this field would be required to have a more in depth and up-to-date understanding of the efficacy of the different approaches available to treat and/or prevent Panic Disorder.

The majority of current scientific understanding point to early and middle adulthood as the stage of life when people later diagnosed with Panic Disorder first experience panic attack. However, there is growing evidence that children and adolescents suffer from Panic Disorder. Blurring and complicating the diagnosis of Panic Disorder in children and adolescents is the high rate of comorbidity between Panic Disorder and one or more anxiety or affective disorder prevalent in this population, e.g., Attention Deficit Disorder with or without Hyperactivity, Generalized Anxiety Disorder, Separation Anxiety Disorder, dysthymia, etc. (Diler et al., 2004; Doerfler et al., 2007; Masi et al., 2000).

Because the bulk of our current understanding, intervention and treatment of Panic Disorder specifically focuses on the adult population, much of the intervention and treatment for children and adolescents who suffer from panic attacks and Panic Disorder are extrapolated from current research on the adult population. The economic cost of Panic Disorder on the individual as well as on the economy in general underscore the need for more studies to be conducted to understand the prevalence of Panic Disorder in children and adolescents, ascertain the possible connection between childhood and adolescent disorders and Panic Disorder, longitudinal studies to understand the connection between childhood disorders and development of Panic Disorder later in life, and possible intervention and treatment designed specifically for this population to help minimize the risk of Panic Disorder in adulthood.


Abrams, K., Zvolensky, M., Dorflinger, L., Galatis, A., Blank, M. & Eissenberg, T. (2008). Fear reactivity to bodily sensations among heavy smokers and nonsmokers. Experimental and Clinical Psychopharmacology, 16(3), 230-239.

Adolphs, R., Tranel, D. & Buchanan, T. (2005). Amygdala damage impairs emotional memory for gist but not details of complex stimuli. Nature Neuroscience, 8(4), 512-518.

Albert, U., Maina, G., Bergesio, C. & Bogetto, F. (2005). Nocturnal panic and recent life events. Depression & Anxiety (1091-4269), 22(2), 52-58.

Allain, H., Bourin, M., Reymann, J., Bentue-Ferrer, D., Patat, A., et al. (1999). Emotion, anxiolysis and memory. Human Psychopharmacology: Clinical & Experimental, 14, S80-S86.

American Psychiatric Association (2000). Diagnostic and statistical manual of mental disorders (4th ed., text revision). Washington, DC: Author.

Amore, M., Magnani, K., Cerisoli, M. & Ferrari, G. (1999, August). Short-term and long-term evaluation of selective serotonin reuptake inhibitors in the treatment of panic disorder: fluoxetine vs citalopram. Human Psychopharmacology: Clinical & Experimental, 14(6), 435-440.

Andlin-Sobocki, P. & Wittchen, H. (2005). Cost of anxiety disorders in Europe. European Journal of Neurology, 12, 39-44.

Bakker, A., van Balkom, A. & Spinhoven, P. (2002). SSRIs vs. TCAs in the treatment of panic disorder: A meta-analysis. Acta Psychiatrica Scandinavica, 106(3), 163-167.

Barlow, D. (1992). Cognitive-behavioral approaches to panic disorder and social phobia. Bulletin of the Menninger Clinic, 56(2), N.PAG.

Beamish, P., Granello, D. & Belcastro, A. (2002). Treatment of panic disorder: Practical guidelines. Journal of Mental Health Counseling, 24(3), 224-246.

Botella, C., García-Palacios, A., Villa, H., Baños, R., Quero, S., Alcañiz, M., et al. (2007). Virtual reality exposure in the treatment of panic disorder and agoraphobia: A controlled study. Clinical Psychology & Psychotherapy, 14(3), 164-175.

Botella, C., Villa, H., García-Palacios, A., Baños, R., Perpiña, C. & Alcañiz, M. (2004). Clinically significant virtual environments for the treatment of panic disorder and agoraphobia. CyberPsychology & Behavior, 7(5), 527-535.

Bouton, M., Mineka, S. & Barlow, D. (2001). A modern learning theory perspective on the etiology of panic disorder. Psychological Review, 108(1), 4-32.

Bowden, C. (1992). Psychopharmacological treatment of panic disorder. Bulletin of the Menninger Clinic, 56(2), 29-41.

Charney, D. (2003). Neuroanatomical circuits modulating fear and anxiety behaviors. Acta Psychiatrica Scandinavica, 108, 38.

Clum, G., Clum, G. & Surls, R. (1993). A meta-analysis of treatments for panic disorder. Journal of Consulting and Clinical Psychology, 61(2), 317-326.

Cox, B., Taylor, S., Clara, I., Roberts, L. & Enns, M. (2008). Anxiety sensitivity and panic-related symptomatology in a representative community-based sample: A 1-year longitudinal analysis. Journal of Cognitive Psychotherapy, 22(1), 48-56.

Dattilio, F. (2001). Crisis intervention techniques for panic disorder. American Journal of Psychotherapy, 55(3), 388-405.

Den Boer, J. (1997, June 2). Defining Panic—a Diagnostic Dilemma. Human Psychopharmacology: Clinical & Experimental, 12, S3-S6.

Diler, R., Birmaher, B., Brent, D., Axelson, D., Firinciogullari, S., Chiapetta, L., et al. (2004). Phenomenology of panic disorder in youth. Depression & Anxiety (1091-4269), 20(1), 39-43.

Doerfler, L., Connor, D., Volungis, A. & Toscano Jr., P. (2007). Panic disorder in clinically referred children and adolescents. Child Psychiatry & Human Development, 38(1), 57-71.

Garcia-Palacios, A., Hoffman, H., Kwong See, S., Tsai, A. & Botella, C. (2001). Redefining therapeutic success with virtual reality exposure therapy. CyberPsychology & Behavior, 4(3), 341-348.

Gassner, S. (2004, March). The Role of traumatic experience in panic disorder and agoraphobia. Psychoanalytic Psychology, 21(2), 222-243.

Goodwin, R. & Gotlib, I. (2004, March). Panic attacks and psychopathology among youth. Acta Psychiatrica Scandinavica, 109(3), 216-221.

Greenberg, P., Sisitsky, T., Kessler, R., Finkelstein, S., Berndt, E., Davidson, J., et al. (1999). The economic burden of anxiety disorders in the 1990s. Journal of Clinical Psychiatry, 60(7), 427-435.

Ham, P., Waters, D. & Oliver, M. (2005). Treatment of panic disorder. American Family Physician, 71(4), 733-739.

Hanisch, L., Hantsoo, L., Freeman, E., Sullivan, G. & Coyne, J. (2008). Hot flashes and panic attacks: A comparison of symptomatology, neurobiology, treatment, and a role for cognition. Psychological Bulletin, 134(2), 247-269.

Hedley, L., Hoffart, A., Dammen, T., Ekeberg, Ø. & Friis, S. (2000). The relationship between cognitions and panic attack intensity. Acta Psychiatrica Scandinavica, 102(4), 300-302.

Heuzenroeder, L., Donnelly, M., Haby, M., Mihalopoulos, C., Rossell, R., Carter, R., et al. (2004). Cost-effectiveness of psychological and pharmacological interventions for generalized anxiety disorder and panic disorder. Australian & New Zealand Journal of Psychiatry, 38(8), 602-612.

Hofmann, S., Meuret, A., Rosenfield, D., Suvak, M., Barlow, D., Gorman, J. et al. (2007). Preliminary evidence for cognitive mediation during cognitive-behavioral therapy of panic disorder. Journal of Consulting and Clinical Psychology, 75(3), 374-379.

Jacobs, W. & Nadel, L. (1999). The first panic attack: A neurobiological theory. Canadian Journal of Experimental Psychology/Revue canadienne de psychologie expérimentale, 53(1), 92-107.

Sainz, K.A.R. (2007). Neurological bases of panic disorder: Selected issues. Psychology Journal, 4(2), 77-90.

Kenardy, J., Robinson, S. & Dob, R. (2005). Cognitive behavior therapy for panic disorder: Long-term follow-up. Cognitive Behaviour Therapy, 34(2), 75-78.

Kohler, C., Carran, M., Bilker, W., O’Connor, M. & Sperling, M. (2001). Association of fear auras with mood and anxiety disorders after temporal lobectomy. Epilepsia (Series 4), 42(5), 674-681.

LeDoux, J. (2002). Emotion, memory and the brain. Scientific American Special Edition, 12(1), 62-71.

Lee, S., Tsang, A. & Kwok, K. (2005). A community-based telephone survey of panic disorder in Hong Kong. Depression & Anxiety (1091-4269), 22(2), 77-83.

Leskin, G. & Sheikh, J. (2002). Lifetime trauma history and panic disorder: Findings from the National Comorbidity Survey. Journal of Anxiety Disorders, 16(6), 599-603.

Lotufo-Neto, F. & Gentil, V. (1994, April). Alcoholism and phobic anxiety: A clinical-demographic comparison. Addiction, 89(4), 447-453.

Marciniak, M., Lage, M., Dunayevich, E., Russell, J., Bowman, L., Landbloom, R., et al. (2005). The cost of treating anxiety: the medical and demographic correlates that impact total medical costs. Depression & Anxiety (1091-4269), 21(4), 178-184.

Masi, G., Favilla, L., Mucci, M. & Millepiedi, S. (2000). Panic disorder in clinically referred children and adolescents. Child Psychiatry & Human Development, 31(2), 139-151.

Masi, G., Toni, C., Perugi, G., Mucci, M., Millepiedi, S. & Akiskal, H. (2001). Anxiety disorders in children and adolescents with bipolar disorder: A neglected comorbidity. Canadian Journal of Psychiatry, 46(9), 797-802.

McDermott, S. (2004). Treating anxiety disorders using cognitive therapy techniques. Psychiatric Annals, 34(11), 858-872.

McLeish, A., Zvolensky, M., Bonn-Miller, M. & Bernstein, A. (2006). Perceived health moderates the association between smoking rate and panic vulnerability variables among daily smokers. Depression and Anxiety, 23(5), 257-265.

Merritt-Davis, O. & Balon, R. (2003). Nocturnal panic: Biology, psychopathology, and its contribution to the expression of panic disorder. Depression & Anxiety (1091-4269), 18(4), 221-227.

Mitte, K. (2005). A meta-analysis of the efficacy of psycho- and pharmacotherapy in panic disorder with and without agoraphobia. Journal of Affective Disorders, 88, 27–45.

Ollendick, T. (1998, September). Panic disorders in children and adolescents: New developments, new directions. Journal of Clinical Child Psychology, 27(3), 234.

Perugi, G., Frare, F. & Toni, C. (2007). Diagnosis and treatment of agoraphobia with panic disorder. CNS Drugs, 21(9), 741-764.

Rivas-Vazquez, R. (2001, February). Antidepressants as first-line agents in the current pharmacotherapy of anxiety disorders. Professional Psychology: Research and Practice, 32(1), 101-104.

Rosenbaum, J. (1990). A psychopharmacologist’s perspective on panic disorder. Bulletin of the Menninger Clinic, 54(2), 184.

Roy-Byrne, P., Craske, M. & Stein, M. (2006). Panic disorder. Lancet, 368(9540), 1023-1032.

Schmidt, N., Lerew, D. & Jackson, R. (1997). The role of anxiety sensitivity in the pathogenesis of panic: Prospective evaluation of spontaneous panic attacks during acute stress. Journal of Abnormal Psychology, 106(3), 355-364.

Schmidt, N. & Smith, J. (2005). Do medications matter in the context of cognitive behavior therapy for panic disorder? Journal of Cognitive Psychotherapy, 19(4), 347-354.

Smits, J., O’Cleirigh, C. & Otto, M. (2006). Combining cognitive-behavioral therapy and pharmacotherapy for the treatment of panic disorder. Journal of Cognitive Psychotherapy, 20(1), 75-84.

Schroeder, B. & Shinnick-Gallagher, P. (2005, October). Fear learning induces persistent facilitation of amygdala synaptic transmission. European Journal of Neuroscience, 22(7), 1775-1783.

Scott, E., Heimberg, R. & Jack, M. (2000). Anxiety sensitivity in social phobia: Comparison between social phobics with and without panic attacks. Depression & Anxiety (1091-4269), 12(4), 189-192.

Smitherman, T. (2005). Challenge tests and panic disorder: Implications for clinical assessment. Professional Psychology: Research and Practice, 36(5), 510-516.

Smits, J., O’Cleirigh, C. & Otto, M. (2006). Combining cognitive-behavioral therapy and pharmacotherapy for the treatment of panic disorder. Journal of Cognitive Psychotherapy, 20(1), 75-84.

Taylor, S. (2001). Breathing retraining in the treatment of panic disorder: Efficacy, caveats and indications. Scandinavian Journal of Behaviour Therapy, 30(2), 49-56.

Van Apeldoorn, F., Van Hout, W., Mersch, P., Huisman, M., Slaap, B., Hale, I., et al. (2008). Is a combined therapy more effective than either CBT or SSRI alone? Results of a multicenter trial on panic disorder with or without agoraphobia. Acta Psychiatrica Scandinavica, 117(4), 260-270.

Vincelli, F., Choi, Y., Molinari, E., Wiederhold, B. & Riva, G. (2000). Experiential cognitive therapy for the treatment of panic disorder with agoraphobia: Definition of a clinical protocol. CyberPsychology & Behavior, 3(3), 375-385.

Zvolensky, M. & Bernstein, A. (2005). Cigarette smoking and panic psychopathology. Current Directions in Psychological Science, 14(6), 301-305.

Zvolensky, M. & Raulin, M. (1999). panic-related fears in persons reporting a family history of panic disorder. Anxiety, Stress & Coping, 12(4), 351.

Zwanzger, P. & Rupprecht, R. (2005). Selective GABAergic treatment for panic? Investigations in experimental panic induction and panic disorder. Journal of Psychiatry & Neuroscience, 30(3), 167-175.