There is no single cause for panic disorder, however, panic disorder has been found to run in families, and suggests 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 like caffeine, in excess, 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 psychodynamically. 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 [http://www.psychweekly.com/aspx/article/articledetail.aspx?articleid=547].

Mediators and Moderators of Panic Disorder

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.

;Smoking

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)[http://www.cdc.gov/nchs/fastats/alcohol.htm] and 7.9% (other psychoactive drugs) [http://www.cdc.gov/nchs/fastats/druguse.htm] 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.

Adapted from the Wikipedia article Panic disorder, under the G. N. U. Free Documentation License. Please also see http://en.wikipedia.org/wiki

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Medical professionals suspecting Münchausen’s in a patient should first rule out the possibility that the patient does indeed have a disease state, but it is in an early stage and not yet clinically detectable. Providers need to acknowledge that there is uncertainty in treating suspected Münchausen patients, so that real diseases are not under-treated. Then they should take a careful patient history, and seek medical records, to look for early deprivation, childhood abuse, mental illness. If a patient is at risk to himself or herself, inpatient psychiatric hospitalization should be initiated.

Medical providers should consider working with mental health specialists to help treat the underlying mood or disorder as well as to avoid countertransference. Therapeutic and medical treatment should center on the underlying psychiatric disorder: a mood disorder, an anxiety disorder or borderline personality disorder. The patient’s prognosis depends upon the category under which the underlying disorder falls; depression and anxiety, for example, generally respond well to medication and/or cognitive behavioral therapy, whereas borderline personality disorder, like all personality disorders, is presumed to be pervasive and more stable over time , thus offers the worst prognosis.

Adapted from the Wikipedia article Münchausen syndrome, under the G. N. U. Free Documentation License. Please also see http://en.wikipedia.org/wiki

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Release of CRH from the hypothalamus is influenced by stress, by blood levels of cortisol and by the sleep/wake cycle. In healthy individuals, cortisol

rises rapidly after wakening, reaching a peak within 30–45 minutes. It then gradually

falls over the day, rising again in late afternoon. Cortisol levels then fall in late

evening, reaching a trough during the middle of the night. An abnormally flattened

circadian cortisol cycle has been linked with chronic fatigue syndrome (MacHale, 1998),

insomnia (Backhaus, 2004) and burnout (Pruessner, 1999).

Anatomical connections between brain areas such as the amygdala, hippocampus, and hypothalamus facilitate activation of the HPA axis. Sensory information arriving at the lateral aspect of the amygdala is processed and conveyed to the central nucleus, which projects to several parts of the brain involved in responses to fear. At the hypothalamus, fear-signaling impulses activate both the sympathetic nervous system and the modulating systems of the HPA axis.

Increased production of cortisol mediates alarm reactions to stress, facilitating an adaptive phase of a general adaptation syndrome in which alarm reactions including the immune response are suppressed, allowing the body to attempt countermeasures.

Glucocorticoids have many important functions, including modulation of stress reactions, but in excess they can be damaging. Atrophy of the hippocampus in humans and animals exposed to severe stress is believed to be caused by prolonged exposure to high concentrations of glucocorticoids. Deficiencies of the hippocampus may reduce the memory resources available to help a body formulate appropriate reactions to stress.

The HPA axis is involved in the neurobiology of mood disorders and functional illnesses, including anxiety disorder, bipolar disorder, insomnia, post-traumatic stress disorder, borderline personality disorder, ADHD, major depressive disorder, burnout, chronic fatigue syndrome, fibromyalgia, irritable bowel syndrome, and alcoholism. Antidepressants, which are routinely prescribed for many of these illnesses, serve to regulate HPA axis function.

Adapted from the Wikipedia article Hypothalamic–pituitary–adrenal axis, under the G. N. U. Free Documentation License. Please also see http://en.wikipedia.org/wiki

No related posts.

Release of CRH from the hypothalamus is influenced by stress, by blood levels of cortisol and by the sleep/wake cycle. In healthy individuals, cortisol

rises rapidly after wakening, reaching a peak within 30–45 minutes. It then gradually

falls over the day, rising again in late afternoon. Cortisol levels then fall in late

evening, reaching a trough during the middle of the night. An abnormally flattened

circadian cortisol cycle has been linked with chronic fatigue syndrome (MacHale, 1998),

insomnia (Backhaus, 2004) and burnout (Pruessner, 1999).

Anatomical connections between brain areas such as the amygdala, hippocampus, and hypothalamus facilitate activation of the HPA axis. Sensory information arriving at the lateral aspect of the amygdala is processed and conveyed to the central nucleus, which projects to several parts of the brain involved in responses to fear. At the hypothalamus, fear-signaling impulses activate both the sympathetic nervous system and the modulating systems of the HPA axis.

Increased production of cortisol mediates alarm reactions to stress, facilitating an adaptive phase of a general adaptation syndrome in which alarm reactions including the immune response are suppressed, allowing the body to attempt countermeasures.

Glucocorticoids have many important functions, including modulation of stress reactions, but in excess they can be damaging. Atrophy of the hippocampus in humans and animals exposed to severe stress is believed to be caused by prolonged exposure to high concentrations of glucocorticoids. Deficiencies of the hippocampus may reduce the memory resources available to help a body formulate appropriate reactions to stress.

The HPA axis is involved in the neurobiology of mood disorders and functional illnesses, including anxiety disorder, bipolar disorder, insomnia, post-traumatic stress disorder, borderline personality disorder, ADHD, major depressive disorder, burnout, chronic fatigue syndrome, fibromyalgia, irritable bowel syndrome, and alcoholism. Antidepressants, which are routinely prescribed for many of these illnesses, serve to regulate HPA axis function.

Adapted from the Wikipedia article Hypothalamic–pituitary–adrenal axis, under the G. N. U. Free Documentation License. Please also see http://en.wikipedia.org/wiki

No related posts.

Medical professionals suspecting Münchausen’s in a patient should first rule out the possibility that the patient does indeed have a disease state, but it is in an early stage and not yet clinically detectable. Providers need to acknowledge that there is uncertainty in treating suspected Münchausen patients, so that real diseases are not under-treated. Then they should take a careful patient history, and seek medical records, to look for early deprivation, childhood abuse, mental illness. If a patient is at risk to himself or herself, inpatient psychiatric hospitalization should be initiated.

Medical providers should consider working with mental health specialists to help treat the underlying mood or disorder as well as to avoid countertransference. Therapeutic and medical treatment should center on the underlying psychiatric disorder: a mood disorder, an anxiety disorder or borderline personality disorder. The patient’s prognosis depends upon the category under which the underlying disorder falls; depression and anxiety, for example, generally respond well to medication and/or cognitive behavioral therapy, whereas borderline personality disorder, like all personality disorders, is presumed to be pervasive and more stable over time , thus offers the worst prognosis.

Adapted from the Wikipedia article Münchausen syndrome, under the G. N. U. Free Documentation License. Please also see http://en.wikipedia.org/wiki

No related posts.