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 a genetic predisposition to alcoholism.
Psychological 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.
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.
There is some evidence to suggest hypoglycemia, hyperthyroidism, mitral valve prolapse, labyrinthitis and pheochromocytoma can cause or aggravate panic disorder.
Prepulse inhibition has been found to be reduced in patients with Panic Disorder.
Stimulants are a rather common cause for panic attacks. An excess of common stimulants such as caffeine.
Many SSRIs also have stimulant side-effects during the beginning of treatment which may exacerbate the condition and have actually caused first-time panic attacks in otherwise healthy individuals being treated for depression.
Flöttmann describes the genesis of panic psychodynamicly. Panic is a stress symptom. Fear is characteristic of each developmental stage because of feeling of guilt or symbiotic binding.
Floating fear or panic stands for the parental stressing call: "Come back to me. You'll panic in your life, you'll have fear of sexuality, fear of separation from me, of being autonomous, and you'll have fear in any situation in your life! You'll feel anxiously, if you do anything that is separating you from mother or father. Don't grow up!" It is the panic that appears in any developmental moment of life.
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 "fight or flight response" mechanism and in return, produces the physiological symptoms that lead to the disorder. Clonazepam, an anticonvulsant benzodiazepine 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.
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.
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, a stimulant, could contribute to panic attacks. However, nicotine withdrawal may also cause significant anxiety which could contribute to panic attacks.
- Alcohol and sedatives
About 30% of people with panic disorder use alcohol and 17% use other 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. Cannabis commonly precipitates panic in panic patients.
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.
While alcohol initially helps ease panic disorder symptoms, medium- or long-term alcohol abuse can cause panic disorder to develop or worsen during alcohol intoxication, especially during alcohol withdrawal syndrome.
This effect is not unique to alcohol but can also occur with long term use of drugs which have a similar mechanism of action to alcohol such as the benzodiazepines which are sometimes prescribed as tranquilizers to people with alcohol problems.
The reason chronic alcohol misuse worsens panic disorder is due to distortion of the brain chemistry and function.
Approximately 10% of patients will experience notable protracted withdrawal symptoms, which can include panic disorder, after discontinuation of benzodiazepines.
Protracted withdrawal symptoms tend to resemble those seen during the first couple of months of withdrawal but usually are of a subacute level of severity compared to the symptoms seen during the first 2 or 3 months of withdrawal.
It is not known definitively whether such symptoms persisting long after withdrawal are related to true pharmacological withdrawal or whether they are due to structural neuronal damage as result of chronic use of benzodiazepines or withdrawal.
Nevertheless such symptoms do typically lessen as the months and years go by eventually disappearing altogether.
A significant proportion of patients attending mental health services for conditions including anxiety disorders such as panic disorder or social phobia have developed these conditions as a result of alcohol or sedative abuse.
Anxiety may pre-exist alcohol or sedative independence, which then acts to perpetuate or worsen the underlying anxiety disorder.
Someone suffering the toxic effects of alcohol abuse or chronic sedative use or abuse will not benefit from other therapies or medications for underlying psychiatric conditions. as they do not address the root cause of the symptoms.
Recovery from sedative Symptoms may temporarily worsen during alcohol withdrawal or benzodiazepine withdrawal.
The World Council of Anxiety does not recommend benzodiazepines for the long term treatment of anxiety disorders due to a range of problems associated with long term use of benzodiazepines including tolerance, psychomotor impairment, cognitive and memory impairments, physical dependence and a benzodiazepine withdrawal syndrome upon discontinuation of benzodiazepines.
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