This article presents current research information on the treatment of panic disorder. Specific guidelines are presented to guide the mental health counselor in the delivery of effective psychopharmacological and cognitive-behavioral treatment.

Panic disorder is a major health problem (Barlow, 1997) and one of the most common psychiatric disorders in the United States. Prevalence rates have been estimated from 3 million to 6 million in the general U.S. population (Foote & Seibert, 1999). Prevalence rates in clinical populations have been reported at approximately 10% (Raj, Corvea, & Dagon, 1993).

The essential feature of panic disorder is the reoccurrence of panic attacks. Panic attacks are sudden episodes of intense fear and apprehension. They can occur independent of specific psychiatric or medical diagnoses. Unlike attacks associated with other anxiety disorders, they are not cued by external stimuli. According to the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV), at least four of the common symptoms of an attack (e.g., shortness of breath, dizziness, heart palpitations, a fear of dying) must be experienced for a diagnosis of panic disorder. One of the panic attacks must be followed by at least 1 month of persistent concern about having additional attacks (American Psychiatric Association, 1994).

This disorder can wax and wane in severity of symptoms and, if left untreated, become chronic and severely reduce an individual's quality of life with disabling health consequences, including increased risk for severe depression and substance abuse (Agras, 1993). There is an increased likelihood of a suicide attempt for individuals with panic disorder. Up to 20% of individuals with panic disorder attempt suicide during their lifetime (Agras, 1993). Individuals diagnosed with substance abuse, depression, or personality disorders are also at risk for developing chronic panic disorder (Bowden, 1992).

Effective and prompt diagnosis and treatment of panic disorder can contribute to a reduction in the chronicity of this disorder. Effective treatment of panic disorder may also result in the reduction in the development of agoraphobia (Michelson, Marchione, Greenwald, Testa, & Marchione, 1996).

Individuals suffering from symptoms associated with panic disorder may seek relief either from a medical or mental health practitioner. These symptoms may either be treated from a medical, psychiatric, or mental health perspective, including psychiatric medication, medical treatment, or any number of therapies. Outcome research supports the treatment of panic disorder from a combination of psychopharmacological and cognitive-behavioral treatments (Beamish et al., 1996; Margraf, Barlow, Clark, & Telch, 1993). Although these accounts report research findings, clear cut clinical guidelines are often missing. The purpose of this article is to delineate the specific strategies identified in the research literature for use by mental health counselors in the treatment of panic disorder.

TREATMENT

Panic attacks differ with regard to frequency, form, and severity from individual to individual and, at times, within the same individual. Full resolution of panic attacks by one form of treatment may not always be possible (Bowden, 1992).

Pharmacological Interventions

Although the prescription of pharmacological treatment is outside the scope of practice of the mental health counselor, knowledge and understanding of effective drug therapy can facilitate the treatment of panic disorder. Clients often present for counseling when they are already taking medications. Information regarding the commonly prescribed drugs, side effects, and recommended dosages is helpful in treating clients with panic disorder. Mental health counselors can better determine when to refer for medication, communicate more effectively with prescribing physicians, and evaluate changes in treatment with this basic knowledge.

There is no clear explanation of the biology of panic. Gitlin (1996) suggests that panic attacks may be a result of exaggerated biological responses to normal stimuli as a result of acute sensitivity and response to internal and/or external cues. According to Katon (1994), physical illness, major life stress, or stimulate medications that increase activity in the brain may trigger the first panic attacks.

Antidepressants and benzodiazepines are the main types of medications found to be effective in the treatment of panic disorder. Selective serotonin reuptake inhibitors (SSRIs), tricyclic antidepressants, and monoamine oxidase (MAO) inhibitors are the main types of antidepressants used in treating panic disorder. Certain SSRIs, tricyclic antidepressants, and MOA inhibitors have been reported in being effective at reducing or eliminating panic attacks (Agras, 1993).

Selective Serotonin Reuptake Inhibitors

Results from recent empirical investigations suggest that SSRIs may be effective in the amelioration of panic symptoms. Although the mechanisms of the SSRIs in the treatment of panic disorder are unclear (Hurst & Harriet, 2000), it is thought that they reduce the sensitivity of some of the receptor sites for serotonin, one of the neurotransmitters involved in emotional regulation (Schatzberg, Cole, & DeBattista, 1997). Fluoxetine (Prozac) has been reported to be effective in blocking panic attacks (Michelson et al., 1998). Several investigations found fluvoxamine (Luvox) to be more effective than placebo or cognitive therapy during 8 weeks of treatment (van Vliet, den Boer, Westenberg, & Slaap, 1996). Other investigations have found setrakline (Zoloft; Pollack, Otto, Worthington, Manfro, & Wolkow, 1998), paroxetine (Paxil; Ballenger, Wheadon, Steiner, Bushnell, & Gergel, 1998), and citalopram (Celexa; Wade, Lepola, Koponen, Pedersen, & Pedersen, 1997) to be more effective than placebo in the treatment of panic disorder. Newer antidepressants such as venlafaxine (Effexor; Pollack et al., 1996) and nefazodone (Serzone; Bystritsky, Rosen, Suri, & Vapnik, 1999) have also been found to be more effective than placebo.

Fluoxetine (Prozac) and fluvoxamine (Luvox) are both serotonin reuptake inhibitors. The major advantages of these new antidepressants are their relative safety in overdose and reduced side effects. Coplan, Tiffon, and Gorman (1993) suggest the use of fluoxetine if the client has been resistant to more conventional pharmacological and psychological treatments. Jefferson (1997) reports that many psychiatrists choose SSRIs as the first line in the treatment of panic disorder. Hurst and Harriet (2000) suggest the use of SSRIs in the short-term treatment of panic disorder.

Recommended dosage and common side effects. People diagnosed with panic disorder may be sensitive to the stimulating properties of SSRIs. However, they are more able to tolerate lower doses than those normally prescribed for the treatment of other disorders and still receive therapeutic benefits (Schatzberg et al., 1996). Roy-Byrne, Wingerson, Cowley, and Dager (1993) recommend an initial dose of fluoxetine at 2 to 5 mg, with a slow increase of 2 mg every 2 to 3 days. If no problems are evident, the medication may increase more rapidly to 10 mg and, within another week, 20 mg if possible (Roy-Byrne et al., 1993). Louie, Lewis, and Lannon (1993) concur that starting fluoxetine at doses lower than 20 mg may be of particular benefit to people with panic disorder. 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 (Massand & Gupta, 1999).

Tricyclic Antidepressants

A select number of tricyclic compounds have been demonstrated to be effective in the treatment of panic disorder (Klerman, 1992). Gitlin (1996) suggests that the efficacy of tricyclics seems to be in the blocking of spontaneous panic attacks. Current hypotheses suggest that these medications decrease the excitability of the brainstem areas regulated by the neurotransmitters norepinephrine and/or serotonin (Gorman, Liebowitz, Fyer, & Stein, 1989). Herrobin (1979) suggests that tricyclic antidepressants block panic attacks by modifying thromboxane and prostaglandin regulated calcium movements. Klein (1967) theorizes that antipanic drugs raise specific releaser thresholds for mechanisms in the central nervous system governing separation anxiety.

Imipramine (Tofranil) and clomipramine (Anafril) have been used frequently in placebo-controlled trials with persons with panic disorder. Ballenger (1986) noted other tricyclics that may be effective in treatment of panic disorder include desipramine (Norpramin), notriptlyine, (Pamelor) and amitriptyline (Elavil). However, studies of those drugs are not as numerous, well designed, or conclusive as those of imipramine. Klerman (1992) reports that the tricyclic antidepressants matprotline (Ludiomil) and amoxapine (Asendin) are most likely ineffective for panic disorder.

The results of several controlled investigations suggest that imipramine is more effective than placebo in treating panic symptoms (Sheehan, Ballenger, & Jacobson, 1980). Other studies with imipramine (Muskin & Fryer, 1981) have resulted in complete cessation of panic attacks.

Recommended dosage and common side effects. The tricyclics generally take up to 8 weeks to become optimally effective (Alexander, 1991). This leads to a high dropout rate from treatment (Uhlenhuth, Balter, Ban, & Yang, 1998). There is common agreement regarding the recommended dosage used in the treatment of panic disorder (Agras, 1993, Noyes, Chaudry, & Domingo, 1986; Sheehan et al., 1980). It is recommended that tricyclic antidepressants, specifically imipramine, be initially administered at a dose of 25 mg at bedtime. Taking the medication in one dose in the evening allows side effects to dissipate during the night. The initial dose should be increased by 25 mg every 3 days, as tolerated, to 150 mg daily. Panic symptoms are generally considered to have a chronic course, and a medication regimen is recommended for at least 6 to 12 months. Medication is gradually reduced until the level required for maintenance is found. As a general rule, medication is reduced once the client is free from panic attacks for 6 months to 1 year (Gitlin, 1996).

Alexander (1991) suggests that the decision to begin tapering medication is important and psychologically complex. Although he suggests that reliance on medication should be avoided, he does suggest that clients must feel ready and confident when tapering begins. In addition, he recommends that clients be well informed about their condition and the possibility of either relapse or withdrawal symptoms. With tricyclic antidepressants, he advises a reduction of 25 mg every 2 to 4 weeks.

Common side effects include an anticholinergic effect often manifested by dry mouth, constipation, blurred vision, or memory difficulties (Noyes, Garvey, Cook, & Samuelson, 1989). A subgroup of clients may become stimulated during the first week or two of medication (Klerman, 1992). In such cases, many individuals find it easier to tolerate the drug with only 10 mg daily or taking the medication earlier in the day (Gitlin, 1996). A benzodiazepine also may be used temporarily to counteract the jitteriness (Noyes et al., 1986). Other side effects may include weight gain, drowsiness, inhibition of sexual functioning, orthostatic hypotension (fall in blood pressure occurring upon standing or standing motionless in a fixed position), light-headedness, and skin rash (Agras, 1993; Klerman, 1992). Klerman (1992) reports that tricyclic antidepressants can precipitate mania in patients with bipolar disorder. Also, tricyclics should only be administered with extreme caution to persons with serious heart disease (Noyes et al., 1989). Considering the high frequency of suicide attempts by clients with panic disorder on imipramine (Bowden, 1992), the risk of overdose is a consideration.

Monoamine Oxidase (MAO) Inhibitors

Jefferson (1997) notes that the MAOs are considered by many to be the most potent antipanic medications. The effectiveness of MAO inhibitors has been demonstrated in double-blind, placebo-controlled trials with phenelzine (Naradil; Agras, 1993), the most studied of the MAO inhibitors used for treating panic attacks (Klerman, 1992). Sheehan et al. (1980) compared phenelzine, imipramine (Tofranil), and placebo in clients with panic symptoms and found no significant differences between the two treatment groups

Recommended dosage and common side effects. There are a number of side effects that have contributed to the decline in the use of MAOs. A tyramine-free diet is necessary with the use of an MAO inhibitor, beginning a day or two before starting the drug and continuing for 2 weeks after stopping the drug (Noyes et al., 1986). Tyramine is found predominately in aged foods such as most cheeses, smoked or pickled fish, fermented meats (summer sausage and salami), red wines, beef or chicken liver, sauerkraut, fava or broad bean pods, and overripe figs or bananas. Other foods and beverages that should be used in moderation while taking MAO inhibitors include canned or packaged soups, soy sauce, alcoholic beverages, yogurt, sour cream, avocados, and raspberries. These foods may precipitate hypertensive episodes (Klerman, 1992). Agras (1993) states that compliance with an MAO may not be as high as with other antidepressants due to the dietary restrictions. The use of MAO inhibitors prohibits the use of many drugs (negative interactions), including most oral antibiotics. The use of alcohol-based products with MAO inhibitors can result in increased blood pressure, headache, and fever.

Withdrawal from antidepressants can produce both physical and psychological distress. Withdrawal symptoms can include influenza-like disturbances, gastrointestinal distress, arrhythmias, sleep disturbance, movement disorders, mania or hypomania, panic attacks, and delirium. Gradual tapering of the medication is suggested to avoid withdrawal symptoms.

Benzodiazepines

Benzodiazepines are used in the treatment of panic disorder. The highly potent benzodiazepines alprazolam (Xanax) and clonazepam (Klonopin) are most used (Agras, 1993). The main physiological effects of benzodiazepines (muscle relaxant, anxiolytic, hypnotic) are the mirror images of major symptoms reported by anxious patients (muscle tension, anxiety, hyper-alertness; Warneke, 1991). Higher potency benzodiazepines are widely prescribed for panic disorder because they are effective and provide rapid improvement (Alexander, 1991). They can be used on an as-needed basis in single doses for clients who experience panic attacks infrequently (Antony & Swinson, 2000).

In a double blind placebo controlled study, Chouinard, Annable, Fontaine, and Solyom (1982) found that alprazolam (Xanax) possessed anti-panic properties. Ballenger et al. (1988) conducted a large, placebocontrolled, 8-week trial of alprazolam in patients with agoraphobia and panic disorder. This drug was found to be effective and well tolerated. At the primary comparison point (week four), 50% of drug recipients vs. 28% of placebo recipients were free of panic attacks.

Noyes et al. (1989) conducted a multicenter placebo-controlled study of the safety, side effects, and patient acceptance of alprazolam (Xanax) for the treatment of agoraphobia with panic disorder. Acceptance of this drug treatment was found to be high, as 84% of the individuals receiving the drug completed the study compared with 50% receiving the placebo. In a double-blind placebo-controlled study, Tesar et al. (1987) reported benzodiazepines superior to placebo and comparable to treatment with tricyclic antidepressants.

Spier, Pollack, Tesar, and Rosenbaum (1986) asserted the efficacy of clonazepam (Klonopin) due to a longer half-life than alprazolam (Xanax). Clonazepam has a prolonged duration phase, which leads to a longer duration of action and is metabolized more slowly (Warneke, 1991). This helps in dosing schedules as clients do not have to take the mediation as frequently as alprazolam (Bowden, 1992). This drug is generally used as a back-up choice for clients that metabolize alprazolam so rapidly that they need to take more than four doses a day (Alexander, 1991). Empirical research of the efficacy of clonazepam is limited. Further studies are in progress on this benzodiazepine in the treatment of panic disorders (Alexander, 1991).

Recommended dosage and common side effects. Relatively high doses of alprazolam (Xanax) are required for the treatment of panic disorder (Bowden, 1992). Agras (1993) suggests that due to its short half-life, alprazolam should be taken every 4 hours during the waking day (three to four times daily) for continuous relief from anxiety. The dosage required for symptom control varies among clients, averaging between 2 and 6 mg/day in most studies. Bowden (1992) has noted that panic symptomotology can recur toward the end of a dosing interval.

Sedation and coordination difficulties are the most common side effects of alprazolam. Tolerance tends to develop within a few days. These problems can be avoided with low doses and gradual increases (Alexander, 1991). Impaired short-term memory is a dosage-related side effect (Bowden, 1992). Possible dependence reactions, including withdrawal and rebound symptoms, are disadvantages with all benzodiazepines (Klerman, 1992). The severity of withdrawal appears less with alprazolam than with other medications studied (Noyes, Garvey, Cook, & Suelzer, 1991). Usually, these effects can be managed with a very slow withdrawal program extending over 2 or 3 months (Agras, 1993). Clients with substance abuse histories may be particularly at risk for dependency problems with benzodiazepines.

Treatment with clonazepam (Klonopin) should begin with .25 mg at each dose, slowly increasing as necessary (Agras, 1993). Davidson (1990) reports that depression appears to occur more frequently in patients taking clonazepam (5% to 10%) than in those taking alprazolam (less than 1%). Warneke (1991) states that clonazepam has fewer side effects than either tricyclics or alprazolam.

There has been a tremendous expansion in the area of psychopharmacological interventions in panic disorder in the past decade. New drugs have been discovered and approved for the treatment of panic disorder. Knowledge in this area can aid counselors in making appropriate referrals, educating their clients, and in realistically evaluating the effectiveness of their counseling (Beamish et al., 1996).

Medications, generally do not cure panic disorder. Rather they allow clients to experience control over their symptoms. Combined treatments with cognitive-behavioral interventions have lower relapse rates over time than treatments with medication alone (Margraf et al., 1993).

COGNITIVE-BEHAVIORAL INTERVENTIONS

Cognitive-behavioral therapy techniques have been found to be effective in treating panic disorder (APA, 1998; Beamish et al., 1996; Overholser, 2000). The cognitive model of panic involves an interaction between physiological responses and cognitive, affective, and behavioral responses (McCarter, 1996). Panic involves activation of the alarm response systems triggered by one of a number of bodily sensations These may be caused in a number of ways, including general sympathetic nervous system overactivity, hyperventilation, increased attention to normal physical sensations, or physical activity (Rapee & Barlow, 1991). These systems are activated simultaneously. This prepares individuals for the fight-or-flight response to danger.

Cognitive responses involve scanning and labeling the danger, affective responses motivate people to respond to the identified danger, and behavioral responses enable deactivation of the alarm system. However, during a panic attack there is no identifiable threat. Therefore, the alarm response becomes associated with harmless elements of the internal and external environments. Individuals with panic disorder misinterpret benign bodily sensations as catastrophizing cognitions and mistaken conclusions. These can maintain panic disorder. A positive feedback loop develops in which the misinterpretation of bodily sensation increases anxiety, which in turn, strengthens the bodily sensations ending in a panic attack (Clark, 1986).

Common cognitive distortions and catastrophic misinterpretations include believing that one will die, is having a heart attack, losing consciousness, or going crazy (Rapee, Mattick, & Murrell, 1986). Such distortions are extremely prevalent among panic-disordered individuals (Ottaviani & Beck, 1987; Rapee et al., 1986). As the individual focuses on these faulty cognitions, panic symptoms escalate (Clark, 1986; Sokol, Beck, Greenberg, Wright, & Berchick, 1989).

The cognitive model of panic asserts that these faulty cognitions can trigger, exacerbate, and sustain arousal. By changing the relationship between physiological arousal and the attributed causes, individuals can view their symptoms in a different context thus eliminating symptoms of panic. In addition, there is evidence that individuals who attribute their panic attacks to catastrophic medical problems, rather than simply manifestations of anxiety, have a significantly more rapid onset of agoraphobia (Breier, Charney, & Heninger, 1986). Therefore, cognitive interventions, which assist individuals in reinterpreting their somatic symptoms of panic, are important components in the treatment of panic disorder.

The behavioral model of panic disorder is based on the classical conditioning paradigm. When an individual is exposed to a threat, anxiety functions as a pattern of increased autonomic activity (Wolpe, 1958). Increased pulse, blood pressure, heart palpitations, dilation of the pupils, nausea, and dizziness are all examples of bodily changes experienced with anxiety. Wolpe (1958) asserts that individuals learn to experience anxiety by association of specific stimuli through classical conditioning. McCarter (1996) suggests that a particular stimulus can become a conditioned cue for panic after only one panic episode. With each subsequent panic episode more and more cues become conditioned and become cues for panic. Somatic processes lead to autonomic arousal and are followed by physiological symptoms causing arousal and creating additional symptoms of panic (Hibbert & Chan, 1989).

Research has focused on the efficacy of some combination of cognitive restructuring, focused cognitive therapy, panic education, guided imaginal coping, breathing retraining and respiratory control, interoceptive exposure therapy, and panic inoculation. Although a definitive statement of which techniques to combine is premature, counseling can be loosely broken into four areas and in the following order:

* Panic education

* Cognitive restructuring

* Respiratory control

* Exposure (McCarter, 1996; Rapee & Barlow, 1991; Sanderson & Wetzler, 1995).

Despite the established efficacy of cognitive-behavioral treatment for panic disorder, the specific mechanisms are still unclear. It may be that repeated exposure to anxiety-provoking stimuli in a systematic manner reduces the anxiety (Rapee & Barlow, 1991). Many of the techniques are designed to help clients cope with anxiety during the exposure component of the treatment.

Panic Education

Panic education generally occurs during the first few sessions. It is based on the assumption that clients need to understand the connection between cognitions and sensations and the development of panic disorder before they can engage in specific therapeutic interventions. The goal is to provide a foundation for developing a new perspective on the panic experience. Therefore, panic education is not intended as a stand-alone treatment, but as an adjunct to other interventions.

Panic-disordered individuals are educated on generic information about panic disorder, often in groups. Information about panic disorder is disseminated and discussed. Some of the information routinely presented includes a definition of panic, common myths about the dangers of a panic attack, and an explanation of the fight-or-flight response (McNally, 1994). Generally, it is explained that panic disorder is a response to stress and anticipatory anxiety a way to ward off a recurrence of a panic attack (Sanderson & Wetzler, 1995). Group sharing of personal experiences of panic is used to help individuals understand that they are not alone in the experience of panic. Clients are provided with success stories about the treatment of panic. Thus, panic education provides information, support, and encouragement as the first step in the treatment of panic disorder (Borden, Clum, & Salmon, 1991).

Counselors may also explore with their clients some of the assumptions and beliefs about the meaning attributed to the panic experiences (McNally, 1994). This may provide a foundation for later changes in beliefs.

Cognitive Restructuring

Cognitive restructuring typically begins during the third and fourth counseling session and continues throughout the course of treatment. It consists of a combination of cognitive techniques and is based on Meichenbaum's (1977) self-coping statement training and Beck's (1988) faulty information processing model of cognition. Cognitive restructuring is based on identifying faulty cognitions and subjecting them to rigorous reality testing (Sanderson & Wetzler, 1995). The goal is to modify the relationship between physiological arousal and the meaning of the arousal (McCarter, 1996). It encourages panic-disordered individuals to question the rationality of their beliefs, and when appropriate, modify their thinking (Clark, 1986).

Treatment begins with an explanation of the cognitive model of panic. Individuals are taught that negative thoughts are capable of increasing anxiety, while positive, adaptive thoughts can decrease it. Inner-dialogue, marked by self-defeating statements, is replaced with more productive statements (Meichenbaum, 1977). The first step in changing the cognitive components of panic is to help clients identify how certain thoughts, beliefs, and assumptions maintain the panic state (McCarter, 1996). This is usually accomplished by a detailed discussion of the last two panic attacks (Sanderson & Wetzler, 1995). This aids the counselor in identifying the individual panic sequence and the panic inducing and maintaining cognitions. Clients may have some initial difficulty identifying cognitions as many have become automatic.

Logs or journals are often used as a form of self-monitoring (Clark, 1986). Initially clients may be asked to keep a simple record of their panic attacks with a numerical rating of their intensity. Simply recording this information may change the client's relationship to the panic. They may feel empowered and the panic may no longer be something to be passively endured (McCarter, 1996).

Clients are taught to reevaluate the validity of their cognitions and to challenge them (Sanderson & Wetzler, 1995). Panic-disordered individuals are instructed to change their negative thoughts, such as "I can't handle this feeling of panic" to more positive adaptive thoughts, such as "I can cope with the anxiety" (Waddell, Barlow, & O'Brien, 1984). Catastrophic misinterpretation of panic-related somatic cues are particularly targeted (Clark, 1986). Disruption of catastrophic interpretations such as having an impending fear of losing one's mind or thinking that one is having a heart attack are challenged and replaced with more self-soothing interpretations, such as "This has happened before, I will live through this." Other common misinterpretations also may be targeted such as overestimating the consequences of a panic attack (public humiliation, losing one's job, interpersonal rejection; Sanderson & Wetzler, 1995).

Sanderson and Wetzler (1995) recommend using logs which target certain areas with clients who have learned how to restructure their cognitions to facilitate the self-monitoring process. In the logs clients are asked to: (a) describe the situation in which the panic attack occurred; (b) specify the feelings at the time of the attack and rate their intensity; (c) in three columns, log the automatic thoughts, the type of cognitive distortion (e.g., jumping to conclusions, overgeneralizations, disqualifying the positive), and a rational (i.e., realistic) response; and, (d) describe the feeling after they completed the log. Often clients continue to keep these logs throughout the course of treatment.

Self-coping statements also can be explored in a rehearsal stage and practiced during the counseling sessions before they are applied to external situations. During sessions, clients are asked to verbalize these positive self-instructional statements, and counselors provide feedback and model alternative statements (Hoffart, 1993).

Finally, counselors work to decatastrophize the situations with their clients. Using a series of questions, a realistic assessment of the worse case scenario is discussed (i.e., "If your worse fears came true would it be as bad as you imagine?")

Thought-stopping and distraction techniques are also included in cognitive restructuring (Agras, 1993). In these instances, clients are encouraged to do something to jolt themselves from focusing on negative thoughts. Having clients splash water on their faces, snap a rubber-band on their wrist, or shout out loud are all techniques that can break the cycle of negative thoughts.

Research suggests that cognitive restructuring is an effective treatment in the reduction of panic attacks (Clark, 1986; Waddell et al., 1984). Selfcoping statements, changing maladaptive thought processes, and disruption techniques have all been used in the treatment of panic disorder.

Breathing Retraining and Respiratory Control

Acute hyperventilation is associated with many panic attacks (Salkovskis, Warwick, Clark, & Wessels, 1986). According to hyperventilation theory, clients with panic disorder experience uncomfortable physical symptoms during attacks that are similar to those produced by hyperventilation such as dizziness, tachyarcardia, palpitations, cold hands, nausea, and breathlessness. During a panic attack, the respiration rate often increases. This is characterized by the use of short shallow breaths (Sanderson & Wetzler, 1995). Studies have shown that individuals who are able to identify and control internal somatic symptoms of anxiety that trigger panic attacks are successful in reducing panic (Beamish et al., 1996).

Breathing retraining is a specific respiratory control technique designed to slow breathing during panic attacks (Rapee & Barlow, 1991). This technique promotes slow, regular breathing and demonstrates to clients that many of the sensations they experience during a panic attack are the result of overbreathing, rather than the actual manifestation of feared conditions. The overall goal of breathing retraining is to reduce the client's respiratory rate (Beamish et al., 1996), decrease the likelihood of hyperventilation, and make it less likely for clients to catastrophize physiological symptoms. The literature suggests that breathing retraining can teach clients to control panic attacks by avoiding hyperventilation when under stressful conditions (Craske & Barlow, 1993; Overholser, 2000; Rapee & Barlow, 1991).

In the first step of breathing retraining, clients are asked to breathe quickly and deeply through their mouths for approximately 90 seconds (Antony & Swinson, 2000; Craske & Barlow, 1993). They are asked to rate the extent to which the symptoms they experience are similar to and different from those experienced during the onset of panic attacks (Clark, Salkovskis, Challey, 1985). The client is asked to elaborate on these similarities and differences with assistance from the counselor. Through exploration with the counselor, the client may be able to identify the similarities between overbreathing and panic attacks. Clark et al. (1985) contend that clients who perceive a similarity between symptoms will likely benefit from this treatment

The second step is to give the client a detailed explanation on how hyperventilation may induce panic attacks (Antony & Swinson, 2000; Craske & Barlow, 1993; Rapee & Barlow, 1991). This explanation includes discussion on how the perceived threat, which triggers this vicious cycle, may come from both external and internal stimuli. While it may seem that the catalyst for an attack may be the perception of some bodily change, an external event may be the actual trigger, which subsequently leads to the physiological symptoms of the attack.

The third stage of breathing retraining teaches clients patterns of breathing that are easily learned, quickly applied in anxious situations, and are incompatible with hyperventilation (Craske & Barlow, 1993). Diaphragmatic breathing is taught by directing the client to inhale into and exhale from the abdomen, rather than the chest. The client's hands may be held on the abdomen to insure proper inhalation and exhalation (de Ruiter, Rijken, Garssen, & Kraaimatt, 1989). A pacing tape for breathing, which provides rhythmic counting for slow, regular breathing, may be developed to guide clients in session and later used at home. Rapee and Barlow (1991) suggest that normal breathing is approximately 10 to 14 breathes per minute. Once the client is able to slow his or her breathing to 10 or less breaths per minute, he or she is encouraged to continue practicing at this speed. The breathing procedure is taught in one counseling session and then practiced repeatedly outside the session until the client is able to apply slow, regular breathing without the assistance of the tape. The final stage of training involves the introduction to interoceptive exposure, where clients induce hyperventilation, experience physiological symptoms of panic, and bring the uncomfortable symptoms under control quickly with slow, regular breathing (Garssen, de Ruiter, & van Dyck, 1992).

Research suggests that breathing retraining is effective in treating panic disorder but appears most effective when paired with cognitive interventions. Research indicates that when breathing retraining is used alone, it is no more effective than a placebo treatment (Garssen et al., 1992; Hibbert & Chan, 1989; Klosko, Barlow, Tassinari, & Cerny, 1990).

Interoceptive Exposure Therapy

Interoceptive exposure is the final component of cognitive-behavioral treatment of panic disorder. It is an intervention based on learning theory and the extinction model. Researchers have suggested that exposure to internal cues, often experimentally induced by hyperventilation or exercise, can alleviate the symptomology experienced with anxiety attacks (Barlow, 1994; Clum & Surls, 1993; Margraf et al., 1993). Studies have shown that individuals who are able to identify and control internal somatic symptoms of anxiety that trigger panic attacks are successful in reducing panic, thus providing support for a behavioral component of panic disorder (Beamish et al., 1996).

Interoceptive cues are the symptom-triggering physical sensations that result in panic. The individual's own physical sensations are capable of triggering a panic attack or increasing arousal and catastrophizing cognitions that can culminate in panic (McCarter, 1996). This suggests that exposure to uncomfortable physiological sensations will eventually extinguish the fear associated with the physical symptoms of panic. Through exposure clients use newly learned coping skills and come to terms with anxiety by altering the psychophysiological responses while in the anxiety state (Sanderson & Wetzler, 1995). Thus, clients with panic disorder can learn to tolerate anxiety without the need to escape, avoid, or escalate into a panic attack. The client and mental health counselor experiment with a number of different exercises to discover those that are effective in recreating symptoms of panic in the client.

Interoceptive exposure combines techniques that attempt to gradually expose the individual to internal physiological cues and confront the physical sensations of panic (Barlow, 1994; Agras, 1993). By using techniques such as bodily spinning, imagery, or hyperventilation, physiological symptoms of panic can be induced (Overholser, 2000). Interoceptive exposure is an appropriate treatment strategy for clients who are especially fearful of the physiological sensations of panic or anxiety.

Interoceptive exposure generally involves three main steps. In the first step, the rationale is presented to the client (Barlow & Craske, 1994; Craske & Barlow, 1993). During this time, clients are provided with the explanation that interoceptive exposure may help decrease fear of physical sensations, just as situational exposure may decrease the fear of activities or objects.

The second step of interceptive exposure involves symptom-induction testing, which establishes what sensations are relevant to the individual's fear and finds appropriate exercises for exposure. The goal of this step is to identify exercises that will create physiological symptoms similar to natural panic. Antony and Swinson (2000) describe a number of exercises that are used in inducing physical sensations for interoceptive exposure. Shaking the head from side to side for 30 seconds is one exercise used in interoceptive exposure. Symptoms may include dizziness, lightheadedness, racing or pounding heart, breathlessness, or smothering feelings. Another example is bending over and placing one's head between one's legs for 30 seconds while sitting, then quickly sitting up; symptoms may include dizziness, lightheadedness, or smothering feelings. Placing a tongue depressor on the back of the tongue is another exercise to induce symptoms. The depressor should stay for a few seconds or until the gag reflex is induced; symptoms may include nausea, racing heart, choking feelings, or gag reflex. Wearing a tie, turtleneck shirt, or a scarf for approximately 5 minutes is another exercise used in interoceptive exposure; symptoms that could be induced by this exercise include tightness in the throat, breathlessness, or feeling smothered. Another exercise involves breathing through a small and narrow straw for approximately 2 minutes; symptoms may include breathlessness, trembling, shaking, chest tightness, choking feelings, racing or pounding heart. Staring at a light for 60 seconds and then attempting to read is another exercise used to induce sensations of panic; symptoms from this exercise may include blurred vision, dizziness, or lightheadedness.

Physiological symptoms can also be reproduced through physical means such as brief, rigorous exercise. For example, clients experiencing dizziness during panic attacks might be spun in chairs. Clients reporting sensations of breathlessness or heart racing might be asked to run up a flight of stairs.

After specific exercises have been chosen, each exercise is demonstrated to the client (Antony & Swinson, 2000). Once the client has attempted each exercise, an interoceptive assessment sheet developed by Barlow and Craske (1994) can be used to report the symptoms of his or her experience, rate the intensity of fear, and rate the similarities between natural fear and panic attacks. Clients who are unsure of which sensations are connected to fear may find this helpful in clarifying which exercises should be used.

In the third step, clients are assigned exercises identified in the preceding step. The client and counselor work together in developing a hierarchy of exercises that induce the least amount of fear to those that induce the most amount of fear. After the hierarchy has been established, the client practices the exercises identified to induce the least amount of fear. The client and counselor continue to practice these identified exercises while gradually working towards the most difficult exercise on the hierarchy. Clients are asked to practice interoceptive exposure between sessions once they have demonstrated their ability to cope with the feelings generated in the presence of their counselor. Sanderson and Wetzler (1995) suggest that a client practice at least three times a week. These sessions continue until the fear has diminished.

Guided imagery can also be used in interoceptive exposure. Guided imaginal coping is one specific type of guided imagery that has been developed for the treatment of panic disorder. The client is exposed to somatic panic symptoms in order to learn to reattribute the misinterpretations. This exposure is done through imagination of situational, somatic, and cognitive stimuli associated with panic attacks (Watkins, Sturgis, & Clum, 1988). Imagined stimuli are matched to client report of actual physical or mental sensations during a panic attack. For example, to mimic physical catastrophes, clients may visualize having a heart attack, fainting, choking, or losing their breath. Mental catastrophes may include imagining loss of control, going crazy, humiliation, or helplessness (Ottaviani & Beck, 1987). After clients are able to imagine their most difficult situation, they then are asked to imagine successfully coping with these situations (Watkins et al., 1988). Coping strategies such as relaxation, cognitive restructuring, and corrective breathing have all been used to treat panic disorder with guided imaginal coping (Borden et al., 1991).

Guided imaginal coping is not well supported in the literature as a standalone technique for the treatment of panic disorder. There is evidence, however, that it may be an effective component when combined with other cognitive and behavioral techniques (Borden et al., 1991). Generally, following imagery work the client progresses to in vivo exposure.

The length of time needed for the fear and panic to diminish (and therefore the specific approach used by the counselor) may differ depending on a number of variables (McCarter, 1996). These include the optimal intensity, speed of exposure, and duration of exposure needed to elicit anxiety, the degree of counselor involvement required, and the type of exposure used (i.e., in vivo, imagery).

The client is assessed for any medical conditions that may affect the safety of some exercises. For example, clients with back or neck problems should not participate in exercises that could exacerbate their conditions such as stationary running or shaking their head. In addition, hyperventilation could aggravate the condition of clients with chronic asthma.

COMBINED TREATMENT

Focused Cognitive Therapy

Focused or focal cognitive therapy is a brief, structured psychological intervention based on the hypothesis that panic attacks are the result of a vicious cycle involving fear of imminent physical or psychological disaster arising from misinterpreted bodily cues. In order to break the cycle, the bodily cues must be reinterpreted (Clark, 1986). Altering the misinterpretations of somatic sensations can markedly reduce the distress associated with the attacks (Rapee et al., 1986).

Treatment begins by educating clients about the cognitive model of panic. The counselor describes how anxiety is a function of perceived threat and how misinterpretations of that threat can maintain panic symptoms (Alford, Freeman, Beck, & Wright, 1990). Next, the client and counselor identify for that individual the exact sequence of bodily sensations and catastrophic interpretations which occur preceding and during a panic attack (Salkovskis, Clark, & Hackmann, 1991). Next, the somatic symptoms are reproduced during counseling, either through verbalizations or imagery.

After the symptoms are induced, whether through imagery or physical methods, clients are encouraged to test the validity of their catastrophic interpretations. Then they are taught to re-attribute their bodily sensations to the proper cause (Salkovskis et al., 1991; Sokol et al., 1989). Selfcoping statements replace the previously employed distorted statements. For example, the idea "I'm having a heart attack" is replaced with "My heart is racing because I ran up the steps" or "My heart is racing because I imagined something that frightens me, but it will soon return to normal."

Salkovskis et al. (1991) recommend that this training during the counseling session be supplemented with homework in the form of a diary. Clients note the occurrence of panic and record the principal sensations experienced as well as any misinterpretations of these sensations and their belief in them at that time of the panic attack. Next, alternative explanations (rational responses) are recorded, followed by a rating of belief in the rational response. Finally, the catastrophic interpretations are re-rated. They found that when catastrophic instances were rated this second time, they were rated significantly less believable than they were initially.

Researchers have found that focused cognitive treatment can reduce panic attacks to zero and significantly reduce misinterpretations of bodily cues after 2 (Salkovskis et al., 1991), 4 (Alford et al., 1990), 8 (Beck, Sokol, Clark, Berchick, & Wright, 1992) and 10 to 26 (Sokol et al., 1989) sessions. There is also evidence that these results are maintained at 1-year follow-up (Beck et al., 1992; Sokol et al., 1989).

Panic Inoculation

Panic inoculation, or panic control treatment, is a multimodal treatment that has received much support in eliminating panic symptoms (Barlow, 1990; Craske, Brown, & Barlow, 1991; Klosko et al., 1990; Shear et al., 1991; Telch et al., 1993). Panic inoculation consists of four basic interventions. The first component is panic education, focusing on the etiology, prevalence, and hypothesized maintenance of panic. Next, cognitive restructuring is added. Clients are encouraged to identify, monitor, and alter their self-defeating statements and negative thoughts that contribute to panic. The third step is breathing retraining to reduce or eliminate physical symptoms that often trigger panic attacks. The final step is the introduction of interoceptive exposure.

Panic inoculation has been found to be significantly more successful in the elimination of panic attacks than progressive relaxation (Barlow, 1990) or a combination of progressive relaxation and panic inoculation (Craske et al., 1991), and as effective as alprazolam (Xanax) without the accompanying side effects of medication (Klosko et al., 1990). The number of required sessions ranges from 15 (Barlow, 1990; Klosko et al., 1990) to between 8 and 24, as needed (Shear et al., 1991). Using panic inoculation in a group format, Telch et al. (1993) were successful in eliminating the panic symptoms after 12 sessions.

TRAINING

Although specialized techniques are used in the treatment of panic disorder this training can be acquired in a self-study program. The information presented in this article is based on current outcome research. We believe we have provided ample information regarding the current psychotropic medications used in the treatment of panic disorder to equip counselors with the minimal knowledge in psychopharmacology to use in treating individuals with panic disorder. The information on the use of cognitive-behavioral treatment provides an outline of the most effective procedures to date. A number of manuals exist that provide detailed explanations of the procedures presented here (see Antony & Swinson, 2000; Barlow & Craske, 1994).

As early as 1974, warnings were given for the use of behavioral techniques such as exposure. Rimm and Masters (1974) strongly suggested that there could be ill effects if caution was not used in their use. Incautious use of exposure can result in the possibility of inadvertent sensitization, in other words, a greater sensitivity to the somatic cues rather than a reduction in anxiety and panic.

Some problems may arise from the amount of time the client is exposed to the physical sensations of panic (Barlow, 1994). The counselor needs to exercise caution to avoid increasing the level of the client's anxiety by inappropriately prolonging the duration of exposure or moving too quickly through the hierarchy (Barlow, 1994; Walker, Hedberg, Clement, & Wright, 1981). An increase in anxiety by the client may result in premature drop out rate (Barlow, 1994). The client's anxiety response may be exacerbated, rather than quelled, if a scene in the hierarchy is terminated too quickly (Walker et al., 1981).

To prevent premature termination of counseling, counselors should take great care in educating clients about treatment procedures. In addition, prior to initiation of counseling, a good rapport between the client and the counselor should be developed and the client's motivation to improve should be strong (Barlow, 1994). A method used to assist motivation is frequent encouragement by the counselor, including pointing out noted improvements between sessions and stressing the importance of continuing treatment, despite any discomfort the client may be experiencing. We recommend that inexperienced counselors follow the manuals verbatim (Rimm & Masters, 1974) and/or seek supervision or consultation when interoceptive exposure is used in treating individuals with panic disorder.

SUMMARY

In summary, there is strong empirical evidence for both psychopharmacological and cognitive-behavioral interventions. Specific knowledge of the psychotropic medications, side effects and dosages can assist the mental health counselor in treating individuals meeting criteria for panic disorder. A combination of specific cognitive behavioral strategies have been identified and elucidated in this article. More research is needed on the efficacy of specific combinations of interventions in the treatment of panic disorder.

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