Comparison of panic disorder with post-traumatic stress disorder (PTSD) in an individual case. An anecdotal account of panic disorder which began in 1991 and was later combined with PTSD in 1999. Emphasis on dramatically differing responses of these two disorders to psychotherapies; including cognitive-behavioral therapy (CBT) and forms of talk therapy. In this single case, psychotherapeutic efforts had no effect on the symptomology and severity of panic disorder yet did have a significant effect on reduction of PTSD over several years. These differences highlight both ends of the physiological-psychological spectrum and demonstrate the extent to which panic disorder is sometimes a very physiological condition. Also emphasized is patient perspectives on distinguishing physiological from psychological symptoms; which can be extremely similar in sensation yet very different in manageability.

Introduction

This case study presents a firsthand comparison of panic disorder with post-traumatic stress disorder (PTSD). Both disorders have well defined onset dates. Though these dates differ by roughly 8-years, the initially occurring panic disorder remained chronic and severe when a traumatic experience resulted in PTSD. Consequently, panic disorder and PTSD were co-morbid and offered a basis of comparison within this single case.

Familial Background

At least three generations of anxiety disorder are known within my family, including both maternal grandparents as well as my mother. Discussions with my maternal grandmother suggest that she has had chronic anxiety most of her life, but only developed panic attacks in her elderly years following her husband's death. Interviews with family members suggest that my maternal grandfather suffered PTSD resulting from an abusive childhood and also from his World War II experience; an American soldier involved in collecting evidence of the Nazi death camps for the Nuremberg Trials.

My mother currently describes her own anxiety disorder as "a consequence of accumulated childhood psychological traumas." She has explained that her anxiety disorder became dramatically acute shortly after my birth in 1963, involving what is currently called 'postpartum obsessive compulsive disorder' with panic attacks. Her symptoms receded in following years to a tolerable and functional form of chronic anxiety which has proved manageable with psychotherapy alone (no pharmaceuticals).

Genealogy (figure 1)

Neither of my paternal grandparents are known to have suffered any psychiatric disorder. They both immigrated from Norway to the United States in the early 1920s and managed to thrive despite many challenges and stressful times.

My father typically had trouble expressing his emotions and suffered notable depression in his later years. However, he displayed no apparent signs of any anxiety disorder. In fact, he enjoyed embracing challenges in both his personal and professional life.

Of my two younger brothers (currently age 34 and 19 years), neither has shown any history of an anxiety disorder or any other psychiatric condition. The first brother shares the same parents as myself. The second brother shares the same mother, but a different father following my mother's second marriage.

Personal Background

Prior to panic disorder and PTSD, my life can be described as reasonably free of medical and psychological disorders. In 1963, I became the first born of three children (currently age 39). Perhaps my most significant childhood problem was some degree of social anxiety which was sometimes described as being a bit "shy." My shyness, however, rarely seemed remarkable to myself or anyone else at the time. I made a few friends as well as participated in Scouts, sports, orchestra, choir and theater. Like most of my peers, I began dating in my early teens. For the most part, I managed an average level of social functionality. Distinguishing between normal childhood insecurity and any possible anxiety disorder is difficult, at best.

Twice during childhood I had experiences that were similar to panic attacks. The first experience was an occasion of collapse (remaining conscious) at about age 10, and the second was an instance of fainting (unconscious for several minutes) at about age 14. These two cases involved spontaneous symptoms similar to panic attacks; including rapidly growing nausea, sweating, dizziness, decreasing muscular strength and control, and anxiety. There were no apparent environmental triggers. At the time, doctors suggested that these episodes could have been isolated attacks of hypoglycemia. Modern endocrinology recognizes that hypoglycemic attacks often produce anxiety, but there appears to be no evidence or models to suggest that anxiety attacks can produce hypoglycemic episodes (1). Nonetheless, my childhood medical tests were unable to confirm hypoglycemia and any relation of these early episodes to my adult panic disorder remains speculative.

The separation and divorce of my parents is important to mention. The separation occurred when I was 12 years old. This was a stressful event that I openly protested at the time. Many future sessions of psychoanalysis focused on this subject, yet no link was ever discovered between it and the sudden onset of chronic panic disorder 15 years later. Furthermore, my first brother (who was age 7 at the time) shared the experience but he never developed an anxiety disorder. Consequently, my parents' separation and divorce appear an insignificant factor in my adult anxiety disorders.

The remainder of my teen years and early adulthood were symptom free with the possible exception of mild social anxiety. During these years, it is important to note that I actively embraced mountaineering, attended Rutgers University, became a president of the physics club, a captain of the chess team and graduated with a degree in physics in 1986; which included minors in mathematics and computer science (including course work in celestial mechanics and artificial intelligence). Following graduation, I spent five years working for Computer Sciences Corporation of which the last three years were spent as a flight dynamics analyst on contract with the National Aeronautics and Space Administration (NASA). I believe these details are important as they demonstrate adventurous and ambitious character traits that oppose common stereotypes of anxiety disorder patients.

Panic Disorder and PTSD Overview

Chronic panic disorder entered my life on January 10, 1991 (age 27). While attending an afternoon seminar, I suddenly suffered a severe "out of the blue" panic attack (symptoms listed in table 1). Coworkers called for paramedics and an ambulance soon took me to the local hospital emergency department. The attack lasted several hours, during which time the emergency department doctors were unable to diagnose the condition. Since this first attack, further attacks were frequent and severe; occurring roughly every other day, often lasting several hours and sometimes resembling seizures. Numerous attempts to diagnose my attacks included examinations by local specialists in medicine and psychology, as well as extensive diagnostic evaluations at Johns Hopkins hospital (Maryland, 1991) and the Lahey Clinic (Massachusetts, 1992).

In the absence of any definitive medical test results, my attacks were originally diagnosed as a form of "stress." At the time, my doctors described this stress as "psychological" in nature and "not a medical problem." Having some experience studying artificial intelligence, I asked if some form of neurological feedback or neurotransmitter problem might be involved? In light of normal test results (Brain MRI, Brain Auditory Evoked Response, office and ambulatory EEG), my doctors dismissed neurological concerns and strongly encouraged psychotherapy. During these first few years, a diagnosis of "panic disorder" was never mentioned; despite its inclusion in the American Psychiatric Association's Diagnostic and Statistical Manual (DSM-III) since 1980.

I embraced both consultations and regular psychotherapy from 1991 to 1998 under a series of psychiatrists and psychotherapists. The first few years of therapy were entirely psychoanalytic and attempted to identify presumed childhood traumas which, hypothetically, were responsible for my attacks. To complement this psychoanalysis, two sessions of regression hypnosis were also conducted. No significant childhood traumas were ever discovered and there was no impact on the severe and chronic nature of my attacks. However, this early therapy was very helpful in managing the depression and suicidal ideation produced by my attacks.

By the mid 1990s, a diagnosis of "panic disorder" was finally suspected. Consequently, my psychotherapy switched modalities to Cognitive-Behavioral Therapy (CBT). Cognitive techniques included the encouragement of positive thoughts, discouragement of negative thoughts and creative use of distraction. Behavioral techniques included regular exposure to agoraphobic challenges as well as deliberate attempts to induce panic attacks. Deliberate attempts to induce panic attacks through hyperventilation, dizziness or other means were entirely unsuccessful. Though prolonged CBT was helpful in managing moderate anxiety and reinforcing optimism, it still had no impact on the severity and frequency of my panic attacks. Likewise, eight months of attending a weekly in-person support group in 2001 had no impact on my panic attacks.

My suspected diagnosis of "panic disorder" was clinically confirmed at the University of Pennsylvania hospital in July 1996. Following a severe attack and visit to the emergency department, I was referred to the university's Outpatient Psychiatric Clinic. The clinic director soon acknowledged that panic disorder can be a "medical problem" rooted in dysfunctions of the nervous system. Consequently, I began my first pharmacological treatment with paroxetine (slowly tapering up to 30-mg/day) and alprazolam (1.5-mg/day). I experienced an immediate and notable reduction in my attack severity, which was attributed to the fast acting alprazolam. After an adjustment period, paroxetine was maintained at 30-mg/day and alprazolam reduced to PRN use only. Relying mainly on paroxetine, my attack severity remained reduced; though still troublesome and with unaffected frequency. However, in 1998, adverse reactions to paroxetine (increasing incidence of sudden fainting, fatigue and a dramatic weight gain of 23-kg) forced me to taper off this medication and rely solely on alprazolam PRN. Fainting, fatigue and weight gain promptly ended with cessation of paroxetine.

My PTSD began on March 26, 1999 (age 35). The triggering event was finding my father's body in his home. My father had been dead about a week and his body was partially mutilated (family pets had removed all the flesh from the head and completely exposed the skull and jawbone). The shock of this discovery immediately produced a variety of symptoms (see table 1). Difficulty with flashbacks set in rapidly. Most flashbacks had obvious triggers; sight or mention of skulls, scent of decay, entering rooms or rounding corners. Flashbacks without triggers occurred in the absence of favorable distractions; mainly when trying to sleep. Diagnosis of PTSD was obvious to both my doctor and myself.

I was unable to afford formal psychotherapy for my PTSD at the time. However, I was able to independently employ some of the same psychological techniques which had been tried on my panic disorder. To perform self-conducted exposure therapy I carefully viewed increasing amounts horror films and war footage which contained triggers; at first for only a few seconds about once a week. Gradually increasing my exposure, I came to tolerate a minute or more over several months, and after a few years my tolerance was up to an hour or more. Common triggers, such as entering rooms and rounding corners, were unavoidable and ensured regular exposure. Also, since I was caring for my father's estate, I was regularly exposed to the scene of the original trauma. In the absence of formal talk therapy, I gradually embraced opportunities to discuss my trauma with family and friends; slowly becoming more open and comfortable with the subject.

Since I had already been using alprazolam to manage panic attacks, it was natural to use alprazolam on a PRN basis to manage attacks of PTSD as well. In addition to minimizing my exposure to the trauma, immediate access to medication helped to manage initial symptoms and possibly limit PTSD severity from the start. However, as I slowly made advances with psychological techniques, my reliance on medication for PTSD attacks correspondingly diminished.

Panic Disorder and PTSD Comparison

When comparing attacks of co-morbid panic disorder and PTSD, it is important to address how such attacks were differentiated. Only by differentiating these two types of attacks can any comparison be made regarding pathology and recovery.

Generally, and in my own experience, attacks of panic disorder are spontaneous, non-triggered events. Typically, the spontaneous nature of such attacks is an important factor in the diagnosis of panic disorder. My own attacks involve rapidly escalating somatic and psychological symptoms (see table 1). The overwhelming cognitive feature was always a frantic sense that I was about to die.

In contrast to panic disorder, my PTSD attacks occurred in two well defined situations. First and most obviously, these attacks were rapidly precipitated by triggers relating to my trauma. Second and less obvious, these attacks also rapidly occurred with the removal of comforting distractions. In either situation, flashbacks relating to the original trauma would precede rapid escalation of psychological and somatic symptoms (see table 1). The overwhelming cognitive feature would be a dreadful anticipation of finding a corpse or even becoming a corpse myself.

Cognitive differences between my attacks of panic disorder and PTSD also have tended to be very subtle. In the case of panic disorder, my attacks consistently produce a sense of my own impending death with thoughts focused on immediate survival. In the case of PTSD, my attacks involved thoughts that focused on the frailty of the human body, the physical state of death, images of mutilation or decomposition and a revulsion at becoming a corpse. Either directly or indirectly, both cases involve thoughts of mortality and therefore have considerable overlap. Nonetheless, I felt a qualitative difference that is hard to describe; perhaps 'a fear of the process of dying' in panic disorder, versus 'a fear of being dead' in PTSD. However, as with my somatic symptoms, these cognitive tendencies were similar enough that I did not consider them a reliable means of distinguishing the two types of attacks.

Distinguishing co-morbid panic disorder from PTSD was primarily made possible through the presence or absence of flashbacks in this case. The flashbacks associated with my PTSD were powerfully intrusive memories of the actual trauma; as opposed to the catastrophic thoughts spawned by such memories. Flashbacks would precede and persist throughout my attacks of PTSD. During prior and co-morbid attacks of panic disorder, such flashbacks were always absent.

Flashbacks also provided useful feedback regarding recovery from PTSD. The time between exposure to a trigger and onset of a flashback and attack gradually increased over several years. This increasing tolerance to triggers was reflected by decreasing severity of PTSD attacks.

Long term comparison of panic disorder and PTSD shows differing responses to psychotherapeutic techniques. The graph below (figure 2) shows a qualitative overview of both disorders in terms of peak severity of attacks; zero representing an absence of anxiety and one representing the worst fear I have ever experienced (seizure-like panic). The majority of attacks were less than peak severity, however peak attacks often occurred within weeks, or days, or even clusters of several per day for both disorders.

Qualitative Overview (figure 2)

The above overview includes treatment strategies over time. Regarding psychotherapies, the first four and a half years were exclusively devoted to psychoanalysis. The following years focused on CBT; at first under the guidance of psychologists and psychiatrists, but eventually conducted without therapeutic guidance due to personal financial limitations. Regarding pharmacotherapy, a first brief attempt with alprazolam was tried in 1992 under the guidance of a general practice doctor. The attempt involved a dosage of less than 1-mg which proved entirely ineffective and was discontinued in less than a week. This experience lead the doctor and I to believe that anxiolytic medication would be ineffective in my case; an impression that would later prove misleading. The first serious attempt of pharmacotherapy began in 1996 under the guidance of psychiatrists; initially trying the combination of paroxetine (a Selective Serotonin Re-uptake Inhibitor or SSRI) and alprazolam (a benzodiazepine or BDZ), but shifting to alprazolam PRN alone in 1999.

Two features of figure 2 are most important in this case study. First, from the beginning of 1999 to the present, both the psychological and pharmacological strategies remained constant. Second, this same period encompasses the co-morbidity of panic disorder and PTSD; during which panic disorder severity remained constant while PTSD severity significantly declined.

PTSD recovery appears to be reflected in the graph below of alprazolam usage (figure 3). Though figure 2 is based on personal observation, figure 3 was computed directly from pharmacy records (2). For each pharmacy refill, the total milligrams per refill was divided by the number of days until the next refill to compute average milligram per day consumption. Since there are sometimes delays or unforeseen complications at the pharmacy, I typically refill my prescription while still having a week's supply of medication and, consequently, there is some degree of error in the computed values. Nonetheless, this refill precaution has been a consistent practice over the time shown in figure 3, so estimating the graph's error is difficult. A very conservative estimate would seem to be an error of 25% of the shown values (on the order of +/- 0.7 to 0.2-mg).

Alprazolam Usage (figure 3)

The dramatic rise in alprazolam usage during mid 1999 can be attributed to a variety of factors. First, use of paroxetine had recently been discontinued and some increase in reliance on alprazolam was to be expected. Second, the traumatic event which caused my PTSD occurred at this time. Third, my attacks of panic disorder had a history of regular surges in both intensity and frequency on a 13-month cycle. This 13-month cycle had been a regular feature of my panic disorder since its onset in 1991. However, the surge in 1999 appears to have been the last as this cycle has been absent in the years since. This cycle and its disappearance remain mysteries, but the chronology suggests a possible interaction between my panic disorder and PTSD. Nonetheless, subsequent absence of regular attack clusters has not diminished the overall severity of my panic disorder.

The general decline in my alprazolam usage since August of 1999 appears to mainly reflect the decline of my PTSD resulting from solo application of CBT techniques. This decline roughly reflects my personal observations of decreasingly frequent flashbacks and growing tolerance to PTSD triggers.

Interpreting Symptoms

Interpreting anxiety disorder symptoms is not yet an exact science. The medical testing necessary to detect possible physiological causes is not commonly available. In the absence of such tests, anecdotal reports can suggest, but not prove, the root cause of an individual's anxiety disorder.

In this case, PTSD and its associated symptoms were almost certainly psychogenic. A well defined traumatic event was responsible for onset. Psychological triggers reliably produced attacks of both psychological and somatic symptoms. Furthermore, psychotherapeutic techniques seem mainly responsible for significant recovery.

In contrast to PTSD, this case of panic disorder and its associated symptoms strongly appear physiogenic in nature. There is no well defined traumatic event responsible for onset. Attacks of both psychological and somatic symptoms lack any clear trigger. Also, long-term application of psychotherapeutic techniques have had no appreciable impact on the severity or frequency of attacks.

Despite the important differences between these co-morbid disorders, some psychological symptoms and many somatic symptoms were effectively identical in both types of attacks. This suggests that even if the root cause of attacks differed significantly, they likely shared some degree of pathology. Regardless of cause, panic disorder and PTSD both involve psychological features. Likewise, research is showing that these disorders also have measurable physiological features as well (3, 4, 5, 6). To label either disorder as purely psychological or purely physiological would be misleading.

Short-term interpretation of symptoms have rarely been good predictors of therapeutic response in this case. Only after years have responses to psychotherapies and medications been somewhat clear. This is a frustrating and daunting reality to a patient like myself who is faced with large investments in psychotherapy and trial-and-error approaches with pharmaceuticals. Indeed, the uncertainties of contemporary treatment strategies can be a significant source of anxiety or stress in themselves.

The symptoms of anxiety disorders can also complicate the diagnosis of other illnesses. As a patient with chronic panic disorder, I am often unable to distinguish whether or not some individual symptoms are anxiety related. Such confusion led to delayed diagnosis and treatment of an eye infection I experienced in 2003; namely, I was uncertain if sleep disturbance and obsession were responsible for perceived eye irritation. Similarly, clinical misdiagnosis can result when diagnostic tests are inconclusive and a doctor must rely strictly upon a symptom profile. Such confusion led one of my doctors to misdiagnose my symptoms as Lyme disease in 1992, which resulted in months of unneeded antibiotic treatments.

Interpreting symptoms also plays a large role in perceptions of disability. In this case, attacks of panic disorder and PTSD have typically been very episodic in nature. During attacks, somatic and psychological symptoms can be extremely crippling. In between attacks, however, there are slices of time where I can manage a significant degree of functionality. Since I am only able to attend appointments or socialize during such slices of functional time, most people don't witness the severity of my attacks and often don't appreciate the full degree of my disability. Beyond the severity of my attacks, inability to predict functional time (when and how long I will be functional) is the greatest cause of disability in my case.

The difficulties involved with interpreting symptoms of anxiety disorders create a strong need for improved diagnostic tests. The ability to determine the type and degree of physiological pathology in the individual patient would greatly aid decisions regarding both psychotherapy and pharmacotherapy. In chronic anxiety disorders, such tests would also help reduce confusion with other illnesses. Furthermore, such tests may also prove helpful when addressing disability issues.

Conclusions

This case study shows that co-morbid panic disorder and PTSD can respond very differently to the same treatment strategy. Personal experience combined with pharmacy records suggest that, in this case, CBT techniques resulted in a significant reduction of PTSD, but had no effect on the severity of panic disorder. A physiological pathology for this case of panic disorder is very likely, yet clinical proof will have to wait for improvements in medical diagnostics.

References

1. J. B. Quintos, M. D., Pediatric Endocrinologist, personal correspondence.

2. Eckerd Drugs, Philadelphia, PA, US, personal pharmacy records.

3. Marshall R. D., Blanco C., Printz D., Liebowitz M. R., Klein D. F., Coplan J. "A pilot study of noradrenergic and HPA axis functioning in PTSD vs. panic disorder." Psychiatry Res. 2002 Jul 31;110(3):219-30.

4. LeDoux, J., "The Emotional Brain: The Mysterious Underpinnings of Emotional Life," Touchstone, New York, NY, 1996. ISBN 0-684-80382-8.

5. Bradwejn, J., Vasar, E., et al, "Cholecystokinin and Anxiety: From Neuron to Behavior," R. G. Landes Co., Austin, Texas, 1995. ISBN 3-540-60132-5.

6. Bremner, J., Randall, P., Scott, T., Bronen, R., et al, "MRI-based Measurement of Hippocampal Volume in Patients with Combat-related PTSD." American Journal of Psychiatry 152, 973. 1995.

Special Thanks

Stuart Shipko, M. D., Panic Disorders Institute, 97 W. Bellevue Dr., Pasadena, CA, 91105, US. http://www.algy.com/pdi

Jay Wesley, Suzan and Marvin Lifschitz, Richard Herman, Steven Eisenberg, Jon Guite, Philip Peters