Panic Disorder

Panic Disorder is an anxiety disorder characterized by recurring severe panic attacks. It may also include significant behavioral change lasting at least a month, and of ongoing worry about the implications or concern about having other attacks. The latter is called Anticipatory Attacks (DSM-IVR). It is important to note that panic disorder is not the same as agoraphobia, although a great deal of people with panic disorder also suffer from agoraphobia.

Panic Disorder is an anxiety disorder characterized by recurring severe panic attacks. It may also include significant behavioral change lasting at least a month, and of ongoing worry about the implications or concern about having other attacks. The latter is called Anticipatory Attacks (DSM-IVR). It is important to note that panic disorder is not the same as agoraphobia, although a great deal of people with panic disorder also suffer from agoraphobia.

Symptoms
Panic Disorder sufferers usually have a series of intense episodes of extreme anxiety during panic attacks. These attacks typically last about ten minutes, but can be as short-lived as 1–5 minutes and last as long as twenty minutes or until medical intervention. However, attacks can wax and wane for a period of hours — panic attacks rolling into one another. They may vary in intensity and specific symptoms of panic over the duration (i.e. rapid heartbeat, perspiration, dizziness, dyspnea, trembling, psychological experience of uncontrollable fear, hyperventilation, etc.). Some individuals deal with these events on a regular basis; sometimes daily or weekly. The outward symptoms of a panic attack often cause negative social experiences (i.e. embarrassment, social stigma, social isolation, etc.). As many as 36% of all individuals with Panic Disorder also have agoraphobia.
Limited symptom attacks are similar to panic attacks, but have fewer symptoms. Most people with PD experience both panic attacks and limited symptom attacks.

Occurrence
Panic Disorder is a serious health problem but can be successfully treated. It is estimated that up to 1.7 percent of the adult American population has Panic Disorder at some point in their lives. It typically strikes in early adulthood; roughly half of all people who have Panic Disorder develop the condition before age 24, especially if the person has been subjected to a traumatic experience. However, some sources say that the majority of young people affected for the first time are between the ages of 25 and 30. Women are twice as likely as men to develop Panic Disorder.
Panic Disorder can continue for months or even years, depending on how and when treatment is sought. If left untreated, it may worsen to the point where the person's life is seriously affected by panic attacks and by attempts to avoid or conceal the condition. In fact, many people have had problems with friends and family or employment while struggling to cope with Panic Disorder. Some people with Panic Disorder may begin to lie to conceal their condition. In some individuals symptoms may occur frequently for a period of months or years, then many years may pass symptom-free. In others, the symptoms persist at the same level indefinitely. There is also some evidence that many individuals (especially those who develop symptoms at an early age) may experience a cessation of symptoms naturally later in life (i.e. past age 50).

Substance Abuse and Panic Disorder
A growing body of evidence exists that shows a link between substance abuse and panic disorder. Several studies have found that cigarette smoking increases the risk of panic attacks and Panic Disorder in young people.[2][3] While the mechanism of how smoking increases panic attacks is not fully understood, a few hypotheses have been derived. Smoking cigarettes may lead to panic attacks by causing changes in respiratory function (e.g. feeling short of breath). These respiratory changes in turn can lead to the formation of panic attacks, as respiratory symptoms are a prominent feature of panic. Respiratory abnormalities have been found in children with high levels of anxiety, which suggests that a person with these difficulties may be susceptible to panic attacks, and thus more likely to subsequently develop Panic Disorder. Nicotine is also a stimulant which could contribute to panic attacks.
Deacon and Valentiner (2000) conducted a study that examined co-morbid panic attacks and substance use in a non-clinical sample of young-adults who experienced regular panic attacks. The authors found that compared to healthy controls, therapeutic alcohol and sedative use was greater for non-clinical participants who experienced panic attacks. These findings are consistent with the suggestion made by Cox, Norton, Dorward, and Fergusson (1989) that Panic Disorder patients self-medicate if they believe that certain substances will be successful in alleviating their symptoms. If Panic Disorder patients are indeed self-medicating, there may be a portion of the population with undiagnosed Panic Disorder who will not seek professional help as a result of their own self-medication. In fact for some patients, Panic Disorder is only diagnosed after they seek treatment for their self-medication habit.

Panic Disorder in Children
A retrospective study has shown that 40% of adult Panic Disorder patients reported that their disorder began before the age of 20. In an article examining the phenomenon of Panic Disorder in youth, Diler et al. (2004) found that only a few past studies have examined the occurrence of juvenile Panic Disorder. They report that these studies have found that the symptoms of juvenile Panic Disorder almost replicate those found in adults – e.g. heart palpitations, sweating, trembling, hot flashes, nausea, abdominal distress, and chills. The anxiety disorders co-exist with staggeringly high numbers of other mental disorders in adults. The same comorbid disorders that are seen in adults are also reported in children with juvenile Panic Disorder. Last and Strauss (1989) examined a sample of 17 adolescents with Panic Disorder and found high rates of comorbid anxiety disorders, major depressive disorder, and conduct disorders. Eassau et al. (1999) also found a high number of comorbid disorders in a community-based sample of adolescents with panic attacks or juvenile Panic Disorder. Within the sample, adolescents were found to have the following comorbid disorders: Major Depressive Disorder (80%), Dysthymic Disorder (40%), Generalized anxiety disorder (40%), Somatoform Disorders (40%), substance abuse (40%), and specific phobia (20%). Consistent with this previous work, Diler et al. (2004) found similar results in their study in which 42 youths with juvenile Panic Disorder were examined. Compared to non-panic anxiety disordered youths, children with Panic Disorder had higher rates of comorbid Major Depressive Disorder and Bipolar Disorder.
Despite the evidence pointing to the existence of early onset Panic Disorder, the DSM-IV-TR currently only recognizes six anxiety disorders in children: Separation Anxiety Disorder, Generalized Anxiety Disorder, specific phobia, Obsessive-Compulsive Disorder, Social Anxiety Disorder(a.k.a. social phobia), and Post-traumatic Stress Disorder. Panic Disorder is notably excluded from this list.
It is also well documented that a person who experiences panic attacks during childhood increases the likelihood of experiencing other anxiety disorders and major depression later in life. Age of onset also appears to impact the occurrence of comorbid disorders. In a study examining children of Panic Disorder patients, Goodwin et al. (2001) found that an early onset of Panic Disorder is associated with increased co-morbid occurrences of Obsessive-Compulsive Disorder, and Separation Anxiety Disorder. In a study conducted by Biederman, Rosenbaum, Bolduc, and Faraone (1991), the authors found that parental Panic Disorder with Agoraphobia increased the risk of their children developing an anxiety disorder later in life. Interestingly, while parental Panic Disorder with Agoraphobia increased the risk of Major Depressive Disorder developing in their offspring, parental depression alone did not increase the risk of their children developing other anxiety disorders. This finding is further supported with later work done by Biederman et al. (2006) in a 5-year longitudinal follow-up study. The authors suggest that the high prevalence of several anxiety disorders in children of Panic Disorder patients provides evidence for a general “anxiety proneness” that may be transmitted from parent to offspring. It was also found that Separation Anxiety Disorder, Specific Phobia and Generalized Anxiety Disorder were the most common anxiety disorders found in the children of parents with Panic Disorder, which is consistent with the findings of Lipsitz, Martin, Mannuzza, and Chapman (1994), who suggested that Separation Anxiety Disorder may be a specific precursor to the development of Panic Disorder later in life. The results of Beiderman et al. (2006) show a pattern in the development of Panic Disorder in which a string of precursor disorders emerge, starting with Separation Anxiety Disorder that eventually progresses to Panic Disorder. For the children in the study, the median age for the first anxiety disorder was 4 years of age. It is clear that not only does Panic Disorder appear to occur in children, but the consequences of early onset Panic Disorder can extend beyond the disorder itself.

Treatment
Panic Disorder is real and potentially disabling, but it can be controlled and successfully treated. Because of the intense symptoms that accompany Panic Disorder, it may be mistaken for a life-threatening physical illness. This misconception often aggravates or triggers future attacks. People frequently go to hospital emergency rooms when they are having panic attacks, and extensive medical tests may be performed to rule out these other conditions, thus creating further anxiety. Nonetheless, Coryell et al found death rates in PD patients exceeded those in the general population. In their study, 20% of deaths in 113 former psychiatric inpatients with PD followed 35 years later were suicides. This study also found that men with PD had twice the risk of cardiovascular mortality compared to men in the general population. Effective treatment of PD has been shown to offset costs of medical care by as much as 94%. Identification of treatments that engender as full a response as possible, and can minimize relapse, is imperative.
Current treatment guidelines American Psychiatric Association and the American Medical Association primarily recommend either cognitive-behavioral therapy or one of a variety of psychopharmacological interventions. Limited evidence exists supporting the superiority of combined treatment approaches. Medication is often not required to treat Panic Disorder effectively. The best first approach is to obtain a reliable psychiatric assessment in order to determine the specifics of your problem. To pursue pharmacological treatment for Panic Disorder, one should visit a psychiatrist. In remote areas, or when a psychiatrist is unavailable, a general practice physician ("family doctor") may be competent to manage the pharmacological ("medications") treatment. A psychiatrist is, by training, better prepared than a general practice physician in pharmacological treatment and should be sought out if available. A psychologist is not a medical doctor and cannot prescribe medication.
There is little evidence that pharmacological interventions can alter phobias, and few studies have been performed. Medications can be used to treat Panic Disorder. Medications can include:
• Antidepressants (SSRIs, MAOIs, tricyclic antidepressants): these are taken regularly every day, and alter neurotransmitter configurations which in turn can help to block symptoms. Although these medications are described as "antidepressants", nearly all of them have anti-panic properties. ). Comorbid depression has been cited as imparting the worst course, leading to chronic, disabling illness.
• Anti-anxiety drugs (benzodiazepines): these drugs should be limited to administration during or at the onset of panic attacks or before challenging/anxiety provoking situations, although there is some evidence that benzodiazepine use can limit the effects of CBT. Some sufferers also take them daily to prevent panic attacks from occurring. These drugs are habit-forming.
A panel of over 50 peer-nominated internationally recognized experts in the pharmacotherapy of anxiety and depression judged benzodiazepines, especially combined with an antidepressant, as the mainstays of pharmacotherapy for anxiety disorders.
Despite increasing focus on the use of antidepressants and other agents for the treatment of anxiety, benzodiazepines have remained a mainstay of anxiolytic pharmacotherapy due to their robust efficacy, rapid onset of therapeutic effect, and generally favorable side effect profile. Treatment patterns for psychotropic drugs appear to have remained stable over the past decade, with benzodiazepines being the most commonly used medication for panic disorder.
Phobic symptoms are often resistant to pharmacological interventions. CBT and one tested form of psychodynamic psychotherapy have been shown to efficaciously treat panic disorder with and without agoraphobia. Clinically, a combination of psychotherapy and medication can often produce good results, although research evidence of this approach has been less robust. Some improvement may be noticed in a fairly short period of time—about 6 to 8 weeks. Thus appropriate treatment by an experienced professional can prevent panic attacks or at least substantially reduce their severity and frequency—bringing significant relief to percent of people with Panic Disorder. Relapses may occur, but they can often be effectively treated just like the initial episode.
In addition, people with Panic Disorder may need treatment for other emotional problems. Clinical depression has often been associated with Panic Disorder, as have alcoholism and drug addiction. More extensive treatment is required for people with treatment-resistant Panic Disorder, which may not respond to many drug or psychotherapies. However, many choices exist, and it is likely that most patients will respond to at least one of the currently available forms of treatment. For patients with panic disorder in New York City or Philadelphia, PA, free high quality psychotherapy is available through a research study, sponsored by the National Institute of Mental Health.
About 30% of people with panic disorder use alcohol and 17% use psychoactive drugs. This is in comparison with 61% (alcohol) and 7.9% (other psychoactive drugs) of the general population who use alcohol and psychoactive drugs, respectively. Utilization of recreational drugs or alcohol generally make symptoms worse (American Psychiatric Association: Practice guideline for the treatment of patients with panic disorder. Most stimulant drugs (caffeine, nicotine, cocaine) would be expected to worsen the condition, since they directly increase the symptoms of panic, such as heart rate. Marijuana commonly precipitates panic in panic patients.As with many disorders, having a support structure of family and friends who understand the condition can help increase the rate of recovery. During an attack, it is not uncommon for the sufferer to develop irrational, immediate fear, which can often be dispelled by a supporter who is familiar with the condition. For more serious or active treatment, there are support groups for anxiety sufferers which can help people understand and deal with the disorder.
Breathing exercises, such as diaphragmatic breathing, can also be found helpful. In some cases, a therapist may use a procedure called interoceptive exposure, in which the symptoms of a panic attack are induced in order to promote coping skills and show the patient that no harm can come from a panic attack.
Interoceptive Desensitization/Symptom Inductions
One particularly helpful and effective form of cognitive behavioral therapy (CBT) is Interoceptive Desensitization. Techniques used may include those based upon the concept that intentional exposure to the symptoms will help decrease the sufferer's fear of panic attacks. In a study by Barlow & Craske (1989), 87% of the individuals that participated in the two of four treatments that involved Interoceptive Desensitization were free of panic at the end of treatment and these results were maintained at a 2-year follow up.
In controlled studies of Interoceptive Desensitization treatments compared to other treatments, those treatments that included Interoceptive Desensitization were found to be significantly superior to other treatments such as muscle relaxation alone, or education or insight-oriented treatments. Indeed, Interoceptive Desensitization often leads to a dramatic reduction in the frequency and intensity of panic attacks and as such should be implemented immediately under the guidance of a mental health professional. It is important the patient is given medical clearance and permission from a medical doctor before attempting these exercises.
Symptom inductions generally occur for one minute and may include:
•Intentional hyperventilation – creates lightheadedness, derealization, blurred vision, dizziness
•Spinning in a chair – creates dizziness, disorientation
•Straw breathing – creates dyspnea, airway constriction
•Breath holding – creates sensation of being out of breath
•Running in place – creates increased heart rate, respiration, perspiration
•Body tensing – creates feelings of being tense and vigilant
The key to the induction is that the exercises should mimic the most frightening symptoms of a panic attack. Symptom Inductions should be repeated 3-5 times per day until the patient has little to no anxiety in relation to the symptoms that were induced. Often it will take a period of weeks for the afflicted to feel no anxiety in relation to the induced symptoms. With repeated trials, a person learns through experience that these internal sensations do not need to be feared—the individual becomes less sensitized or desensitized to the internal sensation. After repeated trials, when nothing catastrophic happens, the brain learns (Hippocampus & Amygdale) to not fear the sensations, and the sympathetic nervous system activation fades.
Causes
There is no single cause for panic disorder, but one thing that is certain is that panic disorder has been found to run in families, and this may mean that inheritance plays a strong role in determining who will get it. It has also been found to exist as a co-morbid condition with many hereditary disorders, such as bipolar disorder, and alcoholism. However, many people who have no family history of the disorder develop it. Malfunctioning of brain structures, such as the amygdala and hormonal/adrenaline glands, may cause an overproduction of certain chemicals and could be source of the physical symptoms.
Other biological factors, stressful life events, life transitions, environment, and thinking in a way that exaggerates relatively normal bodily reactions are also believed to play a role in the onset of panic disorder. Often the first attacks are triggered by physical illnesses, major stress, or certain medications. Some people develop the disorder after using recreational drugs such as marijuana and having a bad experience. People who tend to take on excessive responsibilities may develop a tendency to suffer panic attacks. Post-traumatic stress disorder (PTSD) patients also show a much higher rate of Panic Disorder than the general population. The exact causes of Panic Disorder are unknown at this point.
There is some evidence to suggest hypoglycemia, hyperthyroidism, mitral valve prolapse, labyrinthitis and pheochromocytoma can cause or aggravate Panic Disorder.
Studies in animals and humans have focused on pinpointing the specific brain areas involved in Anxiety Disorders such as Panic Disorder. Fear, an emotion that evolved to deal with danger, causes an automatic, rapid protective response that occurs without the need for conscious thought. This is termed the fight or flight response. It has been found that the body's fear response is coordinated by a small but complicated structure deep inside the brain called the amygdala. Eating disorders have also been linked to have caused panic attacks in several people. Some mood disorders can cause Panic Disorder. In addition to clinical depression, bipolar disorder can cause Panic Disorder in some people. Due to the nature of the fight or flight response many cases of Panic Disorder may be linked with the limbic system and be initiated by those biological factors that could be biological, reinterpreted emotionally as a threat to survival, such as hypoxia (lack of oxygen). If Panic Disorder is experienced more severely during sleep, it would be recommended to have the sufferer evaluated for conditions such as sleep apnea or hypopnea. A sleep-related panic disorder could be most easily distinguished from a night terror by the ability (usually instantaneous) of the Panic Disorder sufferer to regain full consciousness, unlike the night terror sufferer.
Prepulse inhibition has been found to be reduced in patients with Panic Disorder. Disorders with PPI deficits are characterized by a loss of the normal ability to suppress or gate irrelevant sensory, motor or cognitive information. This loss of ‘gating’ may be experienced as intrusive thoughts or sensory information. Reduced PPI and gating functions may be a cause of the heightened state of sensory overload that patients suffering from panic attack often experience.
Stimulants are a rather common cause for panic attacks. An excess of common stimulants such as caffeine and nicotine often can induce panic attacks in less experienced users. Chemicals, including carbon monoxide, in tobacco smoke can also trigger panic attacks in certain people. Some people's response to small amounts of carbon monoxide is to panic. Not surprisingly, the attacks stop or get much less severe after they quit the cause, such as smoking.
Psychological explanations of Panic Disorder have also been put forward. Clark (1986) suggests that Panic Disorder is often caused by "catastrophic misinterpretations", whereby normal bodily sensations, often normal responses to anxiety such as palpitations and sweating, are interpreted as indicating something seriously wrong such as a heart-attack, and this interpretation can be done either consciously or subconsciously. Quite a bit of evidence exists for this theory. For example, activating catastrophic misinterpretations increases anxiety and panic; panic attacks can be reduced as a result of cognitively challenging these misinterpretations; with ambiguous events questionnaires, panic-disorder patients interpret ambiguous sensations more catastrophically than controls. Further, a study by Ehlers et al (1988) which provided false heart-rate feedback to participants found that those with panic disorder react with far greater anxiety.
There are other researchers looking at some individuals with Panic Disorder as having a chemical imbalance within the Limbic System and one of its regulatory chemicals Gaba a. The reduced production of Gaba a sends false information to the Amygdala which regulates the body's "Fright-Flight" mechanism and in return, produces the physiological symptoms that lead to the disorder. Klonopin, a benzodiazapine with a long half-life, has been successful in keeping the condition in check.
Mediators and Moderators of Panic Disorder
Statistically speaking, three criteria are required to identify a mediating variable: First, the independent variable must be statistically associated with the predicted mediator. Second, the predicted mediator must be statistically associated with the dependent variable. Finally, when statistically controlled for in the presence of the mediator, the association between the independent variable and dependent variable must become non-significant (or be significantly reduced in size). A moderating variable is identified when the interaction between the independent variable and the predicted moderator is significant when predicting the outcome variable.
Recently, researchers have begun to identify mediators and moderators of aspects of panic disorder. One such mediator is the partial pressure of carbon dioxide, which mediates the relationship between panic disorder patients receiving breathing training and anxiety sensitivity; thus, breathing training affects the partial pressure of carbon dioxide in a patient’s arterial blood, which in turn lowers anxiety sensitivity. Another mediator is hypochondriacal concerns, which mediate the relationship between anxiety sensitivity and panic symptomatology; thus, anxiety sensitivity affects hypochondriacal concerns which, in turn, affect panic symptomatology.
Perceived threat control has been identified as a moderator within panic disorder, moderating the relationship between anxiety sensitivity and agoraphobia; thus, the level of perceived threat control dictates the degree to which anxiety sensitivity results in agoraphobia. Another recently-identified moderator of panic disorder is genetic variations in the gene coding for galanin; these genetic variations moderate the relationship between females suffering from panic disorder and the level of severity of panic disorder symptomatology.
DSM-IV criteria
DSM-IV diagnostic criteria for panic disorder with (or without) agoraphobia:
A. Both (1) and (2):
1.recurrent unexpected panic attacks
2.at least one of the attacks has been followed by 1 month (or more) of one (or more) of the following:
•persistent concern about having additional attacks
•worry about the implications of the attack or its consequences (e.g., losing control, having a heart attack, "going crazy")
•significant change in behavior related to the attacks
B. The presence (or absence) of agoraphobia
C. The panic attacks are not due to the direct physiological effects of a substance (e.g., a drug of abuse, a medication) or a general medical condition (e.g., hyperthyroidism).
D. The panic attacks are not better accounted for by another mental disorder, such as social phobia (e.g., occurring on exposure to feared social situations), specific phobia (e.g., on exposure to a specific phobic situation), obsessive-compulsive disorder (e.g., on exposure to dirt in someone with an obsession about contamination), post-traumatic stress disorder (e.g., in response to stimuli associated with a severe stressor), or separation anxiety disorder (e.g., in response to being away from home or close relatives).

References
1. "Facts about Panic Disorder". National Institute of Mental Health. Retrieved on 2006-09-30.
2.Pine, D. S., Klein, R. G., Coplan, J. D., Papp, L. A., Hoven, C. W., Martinez, J., et al. (2000). Differential carbon dioxide sensitivity in childhood anxiety disorders and nonill comparison group. Archives of General Psychiatry, 57(10), 960-967.
3.Deacon, B. J., & Valentiner, D. P. (2000). Substance use and non-clinical panic attacks in a young adult sample. Journal of substance abuse, 11(1), 7-15.
4.Cox, B. J., Norton, G. R., Forward, J., & Fergusson, P. A. (1989). The relationship between panic attacks and chemical dependencies. Addictive Behaviors, 14(1), 53-60.
5.Cox, B. J., Norton, G. R., Swenson, R. P., & Ender, N. S. (1990). Substance abuse and panic-related anxiety: A critical review. Behaviour research and therapy, 28(5), 385-393.
6.Diler, R. S., Barmier, B., Brent, D. A., Axel son, D. A., Firinciogullari, S., Chiapetta, L., et al. (2004). Phenomenology of panic disorder in youth. Depression and anxiety, 20(1), 39-43.
7.Biederman, J., Faraone, S. V., Marrs, A., & Moore, P. (1997). Panic disorder and agoraphobia in consecutively referred children and adolescents. Journal of the American Academy of Child & Adolescent Psychiatry, 36(2), 214-223.
8.Essau, C. A., Conradt, J. & Petermann, F. (1999). Frequency of panic attacks and panic disorder in adolescents. Depression and Anxiety, 9, 19-26.

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