Panic Attack Anxiety Disorder

Definition

Panic Attack Treatment

A panic attack is a sudden episode of intense fear that develops for no apparent reason and that triggers severe physical reactions. Panic attacks can be very frightening. When panic attacks occur, you might think you’re losing control, having a heart attack or even dying.

You may have only one or two panic attacks in your lifetime. But if you have had several panic attacks and have spent long periods in constant fear of another attack, you may have a chronic condition called panic disorder.

Panic attacks were once dismissed as nerves or stress, but they’re now recognized as a real medical condition. Although panic attacks can significantly affect your quality of life, treatment is very effective.

Panic Disorder

Panic disorder is different from the normal fear and anxiety reactions to stressful events in our lives. Panic disorder is a serious condition that strikes without reason or warning. Symptoms of panic disorder include sudden attacks of fear and nervousness, as well as physical symptoms such as sweating and a racing heart. During a panic attack, the fear response is out of proportion for the situation, which often is not threatening. Over time, a person with panic disorder develops a constant fear of having another panic attack, which can affect daily functioning and general quality of life.

Panic disorder often occurs along with other serious conditions, such as depression, alcoholism, or drug abuse.

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Genetic and family studies

Clinical experience with patients revealed that PD seems to run in families and have a genetic component. These findings led to epidemiological studies investigating the incidence of this disorder in families of the patients. Despite methodological differences and variations in the definitions of the disorder as well as the target population of the anxious patients, the results seem to be relatively consistent. Carey and Gottsman (1981) studied families of probands with anxiety disorders and found that 15% of the first-degree relatives also suffered from anxiety disorders. A more pertinent study by Crowe et al. (1983) focused on panic disorder. Around 25% of the first-degree relatives of PD patients received the same diagnosis, as compared to 2.3% of relatives of normal controls.

Studies with twins who grew up together can also provide us with a useful piece of information. In Slater and Shields’ study (1969), monozygotic twins had concordance rate of 41% for anxiety states, whereas the concordance among dizygotic was only 4%. Torgersen (1983, 1990) investigated concordance rates for anxiety disorders with panic attacks and found that 31% of the monozygotic twins had a similar diagnosis compared to 0% of the dizygotic twins. When he narrowed down the comparison to PD with agoraphobia, the concordance rate between monozygotic twins was 15%. Even though the differences in concordance rates might appear important, they might be misleading. First of all, the number of subjects was small, such that, for example, the concordance rate of 31% in monozygotic twins was based on 4 out of 13 pairs of twins, which is obviously not enough to generalize. Secondly, the higher concordance in monozygotic twins could be potentially explained by other non-genetic factors. For instance, monozygotic twins may be treated differently by their parents, extended families and peers. They might have more profound identity crisis than the one that teenagers usually go through. Often they are dealt with as an entity rather than two separate individuals. In addition to this, they might tend to develop mutual dependency and have more experiences of separation anxiety, a state that seems to be related to agoraphobia and panic disorder.

Neurochemistry of PD

The evidence for neurochemical pathology in PD comes from numerous sources: challenge studies, effects of antipanic medication, biochemical comparisons of PD population with healthy subjects in terms of reactivity and basal levels, brain imagery and animal experiments. Several major hypotheses, explaining the neurochemical bases of PD, have been formed and supported by evidence.

One of the most intriguing hypotheses postulates an abnormality of the noradrenergic and adrenergic systems. Increased plasmatic and urinary concentrations of epinephrine (EPI) and norepinephrine (NE) in panic disorder patients have been shown in some but not all studies (Braune et al., 1994; Butler et al., 1992; Villacres et al., 1987; Nesse et al., 1985a; Appleby et al., 1981; Wyatt et al., 1971; Cameron et al., 1984). In addition, augmentations of plasma 3-methoxy-4-hydroxyphenylethylene (MHPG), a metabolite of NE, have been documented in patients with frequent and severe panic attacks (Charney et al., 1984b). Panic patients confronted with anxiogenic situations have increased plasma free MHPG and NE levels (Braune et al., 1994; Ko et al., 1983; Uhde et al., 1982; Nesse et al., 1985b). Stimulation of the noradrenergic system by alpha2-adrenoceptor antagonist yohimbine and beta-adrenoceptor agonist isoproterenol produces panic-like symptoms in PD patients and some healthy subjects (Charney et al., 1987; Charney et al., 1990; Pohl et al., 1990). Pathological changes in the alpha or/and beta-receptors have been demonstrated (Charney & Heninger, 1986; Rainey et al., 1984; Nesse et al., 1984; Pohl et al., 1985).

Another plausible hypothesis concerns serotonergic system, especially in terms of interaction with noradrenergic system (Zacharko et al., 1995). Raphй nucleus, a midbrain structure with high concentration of serotonergic neurons, projects to locus ceruleus, and has an inhibitory influence on the activity of noradrenergic neurons (Meltzer, 1987). Pharmacological agents that decrease serotonergic activity have anxiolytic effect in animals (Briley et al., 1990). Serotonin and its metabolite 5-HIAA are reduced in anxious dogs (Guttmacher et al., 1983). In humans, alleviation of symptoms is achieved by administration of selective serotonin reuptake inhibitors. Murphy & Pigott (1990) have presented evidence suggesting that the anxiolytic effects of benzodiazepines might also be related to serotonergic activity. In addition to it, panic disorder patients reported an exacerbation of symptoms when they received serotonin precursors tryptophan and 5-HTP, serotonin receptors’ agonist m-chlorophenylpiperazine and flenfluramine, a drug that increases the synaptic availability of serotonin (Murphy & Pigott, 1990, Den Boer & Westenberg, 1990, Targum, 1990, Kahn & Van Praag, 1988). It is thus possible that an altered serotonergic transmission is one of the elements that are implicated in anxiety and panic.

Another major hypothesis for PD etiology involves benzodiazepine receptors and their natural ligands. The anxiolytic action of benzodiazepines is mediated through benzodiazepine receptor complex, potentiating the inhibitory effects of GABA (Lima, 1991; Paul & Skolnick, 1981; Skolnick & Paul, 1982). Sensitivity of central and peripheral benzodiazepine receptors have been shown to be modified by aversive life events and social variables (Trullas & Skolnick, 1993). Studies have demonstrated that animals with low exploratory behavior (anxious) have lower density of brain benzodiazepine receptors (Rago et al., 1991). Also, stimulation of benzodiazepine receptors by their inverse agonists, beta-carbolines, produces anxiety and panic-like symptoms in PD patients and healthy subjects (Zacharko et al., 1995).

What Causes Panic Disorder?

Panic Disorder

Although the exact cause of panic disorder is not fully understood, studies have shown that a combination of factors, including biological and environmental, may be involved. These factors include.

Family history. Panic disorder has been shown to run in families. It may be passed on to some people by one or both parent(s) much like hair or eye color can.

Abnormalities in the brain. Panic disorder may be caused by problems in parts of the brain.

Substance abuse. Abuse of drugs and alcohol can contribute to panic disorder.

Major life stress. Stressful events and major life transitions, such as the death of a loved one, can trigger a panic disorder.

How Common Is Panic Disorder?

Panic disorder affects about 2.4 million adult Americans. Panic disorder most often begins during late adolescence and early adulthood. It is twice as common in women as in men.

How Is Panic Disorder Diagnosed?

If symptoms of panic disorder are present, the doctor will begin an evaluation by performing a complete medical history and physical exam. Although there are no laboratory tests to specifically diagnose panic disorder, the doctor may use various tests to look for physical illness as the cause of the symptoms.

If no physical illness is found, you may be referred to a psychiatrist or psychologist, mental health professionals who are specially trained to diagnose and treat mental illnesses. Psychiatrists and psychologists use specially designed interview and assessment tools to evaluate a person for panic disorder.

The doctor bases his or her diagnosis on reported intensity and duration of symptoms, including the frequency of panic attacks, and the doctor’s observation of the patient’s attitude and behavior. The doctor then determines if the symptoms and degree of dysfunction suggest panic disorder.

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Panic Attacks Guide

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Help To Stop a Panic Attack

Due to the nature of a panic attack, treatment can be difficult. Panic attack treatment is varied because the symptoms are. Symptoms tend to vary from heart palpitations, restrictive breathing, to hot flushes. For this very reason, diagnosis of the condition can be difficult, and until recently it was uncertain that the condition existed at all. More often than not, it was brushed aside, believing it was stress related and nothing more.

Recent studies have shown, it is a very real and often serious condition which leaves the person feeling debilitated and unable to cope with what’s happening to them. Have you ever felt extremely anxious? Have you felt your heart rate is elevated above normal, and experienced hot-flushes? If yes, then you’ve most likely experienced a panic attack. You would have felt overwhelmed by sudden anxiety, and find yourself trying to look for drastic ways to try and calm your self down. The causes for a panic attack are often varied and sometimes unknown, but is most often related to high stress levels and even substance abuse as the most common causes.

Ways to stop panic attacks do vary. They tend to be either chemical treatments, psychological, or natural. Many of the chemical, drug, treatments are similar and all contain the same chemical, benzodiazepine, in them. All the variants have a sedatory effect on the nervous system, calming the person down quickly and effectively. However, the side effects can be anything from hallucinations to apathy, and might even result in addiction after long periods of continuous use. Instead of such strong measures, psychologists often prescribe anti-depressants, in order to assist treatment. The reason being, by regulating Serotonin and Dopamine levels in the brain, the person will become more relaxed and happier with life. This means there is less reason for an attack.

Psychological counseling for panic attack treatment is also common. The person spends some time talking to a professional, trying to work through their problem. Behavioral therapy like this, can emphasize a person’s state of mind, when the attacks occur. By giving sufferer’s better understanding, of what is actually happening to them, they become more able to reason with themselves during an attack. Thereby controlling the symptoms more effectively.

Natural remedies seem to be just as effective, but rely heavily on the individual’s ability to work through it. Anxiety often causes rapid breathing and by breathing into a paper bag, it will reduce the breathing rate and the amount of oxygen intake. This can calm the person down.

A panic attack is a feeling of intense anxiety and impending doom in the absence of circumstances that justify these feelings–it’s easy to define, but not at all easy to live with. Long-term treatments may involve medication and therapy. In the short term, however, a few simple techniques can help you end your panic attack in just a few minutes. Follow these steps to find out how.

Difficulty:Moderately ChallengingInstructions

1

Recognize that you’re having a panic attack. You’re not really in any danger. You’re not losing your mind.

2

Don’t leave the situation. You will only condition yourself to have another panic attack the next time you are in that situation.

3

Focus on something outside yourself. Find the nearest object, grab hold of it and start talking. Describe its color, smell and texture. Talk about how it came to be near you, how you feel about it or what its purpose is. Keep talking until the attack ends.

4

Breathe deep. You’ll need to start practicing this technique well in advance, perhaps with the help of a therapist. The idea is to keep your chest still and let your abdomen expand with each breath, stretching your diaphragm. Exhale slowly through pursed lips.

5

Seek help. Whatever the reason for your panic attacks, there’s no shame in getting help from a medical doctor or a psychotherapist. Often, it only takes a few therapy sessions to get relief from panic attacks.

person who is experiencing panic attacks knows that this come in a surprise without the slightest indication. So how to you stop panic attacks to happen and just leave you helpless just like that? It is important and helpful to know how to stop panic attacks because you know that this kind of untoward situation may lead to a more serious damaging one.

Most of the time people who are experiencing the said problem feels extreme fear while / during the attack. This is true no matter how many times did the person felt it happen to them. To stop panic attacks, see the helpful tips on how to go about it. Knowing some ways to treat your problem while having it will somehow give you that needed peace of mind that may calm yourself and eventually stop panic attack.

In order for you to know if you are already experiencing the attack, see the most common signs and symptoms of it below:

• You are already hyperventilating

• You are having difficulty in swallowing. You even feel a choking sensation and smothering sensation.

• Your body is suddenly developing sweat all over.

• You are experiencing pain in the following: chest and stomach.

• You are losing your actual personal identity.

These are not very serious symptoms of the said disorder. You can easily fight these if you start by calming yourself.

It may also help if you know what is triggering the attack. Once you are able to determine it, it should be easy for you to know how to treat or stop the panic attack.

To know some of the most common triggering factors of panic attack, see the details below:

1. Due to genetic reasons.

2. Medical reasons. People who have heart problems are the most common to feel panic attacks.

3. Phobias that may stress the person’s mind.

4. An experience that gave trauma to the person.

People who have this kind of disorder can only handle a specific amount of stress. Anything that goes beyond it will surely cause the attack.

The best way to stop panic attack in general is to avoid the stressful situations that may trigger your body and mind to panic. It may help if you can meditate and relax yourself while you are having the attack. Doing this will help you release the pressure you are feeling inside that tightens you breath and chest. This will also help you calm yourself and have a focused mind easily.

Once you are able to relax yourself and have stopped the panic attack, don’t think that you can leave what happened just like that. It is already an indication that you need to seek a professional advice from a doctor who specializes in the field of treating people who have the said disorder. Your doctor will give you the best advices on how to go about the prevention of the untoward condition and prescribe medications too that may help ease the pain and calm yourself to stop panic attack.

What Are the Treatments for Panic Attacks?

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The cause of most panic attacks is not clear, so treatment may be different for each person. Medication is used for prevention and/or immediate alleviation of symptoms and is usually the main line of treatment. In addition, psychotherapy, cognitive-behavioral therapy, relaxation, and/or meditation are often used to help relax the body and relieve anxiety.

If you’re in the middle of a panic attack, immediate relief of anxiety symptoms can come from sedative type antianxiety medications such as Xanax, Klonopin, and Ativan. These drugs are provided at least in the beginning of medical therapy, but are not for long-term use.

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Antidepressants often help prevent anxiety and reduce the frequency and severity of panic attacks, but are not used for immediate relief during an attack. Frequently used antidepressants are the selective serotonin reuptake inhibitors (SSRIs, such as Prozac, Paxil, Celexa, Lexapro, and Zoloft). This group of medications is often considered the first line of treatment for panic disorders.

For preventive or maintenance care, psychotherapy offers support and helps minimize fear. In some cases, psychotherapy alone can clear up the disorder.

Cognitive-behavioral therapy helps people learn to deal with panic symptoms, using techniques like muscle and breathing relaxation. Patients also gain reassurance that panic will not lead to the catastrophic events they fear, since many people fear they are having a heart attack or going crazy.

Important note regarding medications: Some of these drugs can actually produce the anxiety symptoms of a panic attack. It is often best to start with a low dose and slowly increase medication for this disorder.

How Can I Prevent Panic Attacks?

Anxiety Attacks Vs Panic Attacks

You can take steps to lessen the chance of having panic attacks and learn to manage them better. Learn to recognize a panic attack. When you sense the first symptoms, know that other symptoms may follow. You have survived them before and can do so again. Try slow, deep breaths.

Take your time. It’s important not to hope for a quick cure. Therapy takes time, and improvement comes in small steps.

Go easy on yourself. People who feel panic tend to be overly critical of themselves.

Learn to lower your level of everyday anxiety through a variety of techniques, including meditation and exercise.

Learn other relaxation techniques, like deep breathing or guided imagery.

Avoid stimulants, such as nicotine and caffeine, which can be found not only in coffee, but many teas, colas, and chocolate.

Anxiety and Panic Attacks

The essential assumption of the biomedical model is that mental illness is basically a biological disease. In other words, the etiology of the mental disorder can be explained by physical causes, such as infections, genetics, neuroanatomic pathology or malfunctioning biochemistry. Evidence has accumulated, demonstrating that PD may be viewed as a biological disease.

Panic symptoms are physical in nature

The onset of symptoms is abrupt, reaching peak within minutes. It rapidly subsides, leaving only residual anxiety. Typically, the PA come out of nowhere, even though some patients experience situationally bound and situationally predisposed PA. Often, patients are unable to identify anything that could possibly trigger a PA. They experience PA watching cartoons, playing with their children, resting etc., simply put, in situations that do not present any stress or threat to them.

The physical nature of the symptoms of panic attack also provides some reasons for the claim that PA/ PD involves biological modifications. The PA symptoms correspond to a great degree to symptoms of acute activation of the sympathetic branch of the autonomous nervous system, typical for the fight or flight reaction. Indeed, several authors argue that panic attack is, in fact, a fight or flight reaction of the body in absence of a real danger (Rosenhan & Seligman, 1989). When confronted with a real or perceived threat, the automatic “fight or flight” response may be triggered to prepare the body for immediate action. This response is accompanied by peripheral secretion of catecholamines, especially epinephrine and norepinephrine, and glucocorticoids (Carlson, 1992). These hormones increase the availability of the body’s energy by glycogenolysis in liver and skeletal muscles thus raising the blood glucose and lactate, lipolysis in adipose tissue, mobilization of free fatty acids, and by increasing temperature. Both epinephrine and norepinephrine also dilate coronary blood vessels. As a consequence, the rate and strength of the heartbeat increases to supply more oxygen to the tissues. While norepinephrine produces vasoconstriction in skin, mucosa, skeletal muscles and most other organs, epinephrine dilates veins in skeletal muscles. These effects result in hypertension and consequently in reflex bradycardia. Other symptoms of a sympatho-adrenergic stimulation involve modifications of breathing, increased temperature, localized sweating, decreased motility and tone of stomach and intestine, constrictions of sphincters in stomach and intestine as well as piloerection. Breathing increases in rate and depth to exchange more oxygen to prepare for exertion. Breathlessness, dizziness, and pain or tightness in the chest may be experienced. Sweat glands are stimulated to prevent overheating. The pupils of the eye dilate to admit more light and increase peripheral vision to scan for danger. Sensitivity to bright light, and visual disturbances may occur. The digestive system shuts down to conserve blood for the muscles. A dry mouth, nausea and constipation may result. Muscles tense to prepare for flight, but may cause spasms and trembling when action is not taken. This complex response was developed through evolution in many organisms and normally serves for survival and protection. As mentioned above, symptoms of sympathetic activation and symptoms of panic attack share many common symptoms. Therefore, panic attack may be viewed as an emergency response which occurs in a situation where it is not appropriate (Barlow & Craske, 1994).

Antidepressant and antipanic drugs are efficacious in treatment of PD

Another argument for the biological hypothesis of PD is that pharmacotherapy is efficacious in treatment of PD. Several classes of drugs are being used in PD patients, namely the benzodiazepines, tricyclic and heterocyclic antidepressants, monoamine oxidase (MAO) inhibitors, reversible MAO inhibitors and selective serotonin reuptake inhibitors (SSRI). Except for benzodiazepines, all anti-panic drugs are in fact antidepressants, and act on the aminergic systems (Taylor & Arnow, 1988). Benzodiazepines act on the GABA-receptors. If PD had no biological bases, its symptoms could not be alleviated by medication. Whatever the type of medication, efficacy of drugs to treat PD implies that the underlying mechanism of development or symptomatology is biological.

Frequency and intensity of PA varies during menstrual cycle and pregnancy

Clinical and scientific evidence exists demonstrating that gonadal hormones have a strong influence on PD, especially in terms of frequency and intensity of PA. Spontaneous panic attacks rarely start before puberty or after menopause, suggesting that, in women, occurrence of PA may be linked to production of female reproductive hormones (Klein et al., 1992). Premenstrual exacerbation of panic symptoms has been documented (Breier et al., 1986; Cameron et al., 1988). Several authors reported that women with LLPDD are more sensitive to panic-provocation procedures (Harrison et al., 1989; LeMellйdo et al., 1996). In addition, panic rate in women with or without LLPDD increases when they are challenged during the luteal phase, the LLPDD patients having a higher rate (Sandberg et al., 1993; LeMellйdo et al., 1996). This phenomenon is attributed to a drop in progesterone levels before the onset of menses, the women with largest progesterone fluctuation being most vulnerable (Halbreich et al., 1986).

Clinically, a marked decrease of panic has been observed during pregnancy and lactation, with postlactational exacerbation of symptoms. These changes most likely reflect increased levels of progesterone, estrogen and oxytocin during pregnancy or lactation (Klein, 1993). The fact that the condition of PD patients improves during this time is a strong argument for the biological view of PD. As Klein points out, pregnancy and childbirth present an increased vulnerability, marked by heightened threatening endogenous stimuli. According to cognitive theories, which postulate that PA result from catastrophic interpretation of physiological changes, such states should make patients more prone to panic. Apparently this is not the case (Klein, 1994).

Experimental procedures (challenge) reproduce panic attacks in laboratory

For nearly three decades, researchers have been using various procedures in order to reproduce the emotional, cognitive, physiological and neurochemical changes accompanying panic attacks. Among the first agents used to trigger anxiety-like symptoms were epinephrine and norepinephrine (Wearn & Sturgis, 1919; Lindemann, 1935; Lindemann & Finesinger, 1938). Cholinergic agents, such as cholinomimetic mecholyl and cholinesterase inhibitor physostigmime, were also used in several studies (Lindemann & Finesinger, 1938; Risch et al., 1981; Paul & Skolnick, 1981) One of the most researched panic-provoking pharmacological agents is sodium lactate (Pitts & McClure, 1967; Haslam, 1974; Appleby et al., 1981; Liebowitz et al., 1984). Voluntary hyperventilation and carbon dioxide have frequently been used to study the underlying mechanisms of panic attack (Van den Hout & Griez, 1984; Gorman et al., 1984; Papp et al., 1989). Caffeine challenge induces anxiety-like symptoms suggesting a possible implication of the adenosine system in panic anxiety (Charney et al., 1984a; Uhde, 1990; Boulenger et al., 1984). The administration of cholecystokinin tetrapeptide (CCK4) has also been used in several recent studies (Bradwejn and Koszycki, 1994a; Bradwejn & Koszycki, 1994b). Several other panic-provocation agents, such as yohimbine, isoproterenol, piperoxan act on the noradrenergic or adrenergic systems (Olpe et al., 1983, Charney et al., 1987; Charney et al., 1990; Pohl et al., 1990).

These procedures are a valuable tool for the experimental evaluation of neurochemical correlates of panic attack symptoms. They are capable of inducing experience that is phenomenologically similar to spontaneous panic attacks, as pointed out by panic patients. Therefore, a phenomenon which can be reproduced by pharmacological means must have biological bases.

Non-fearful and limited symptom panic attacks

Many panic patients report experiencing so called limited symptom panic attacks, which are characterized by presence of less than four symptoms, and, importantly, absence, or low levels of anxiety. Limited symptom panic is often seen in patients undergoing pharmaco or psychotherapy. Some patients experience panic attacks without fear, which may contain several physical symptoms without the emotional and cognitive components of PA . The mere existence of this phenomenon points to biological bases of PD.

PA may be triggered or aggravated by use of drugs

Many patients can trace the onset of panic attacks to the use of drugs, especially cocaine and amphetamines. Both of these drugs alter the noradrenergic function (Taylor & Arnow, 1988). The fact that drugs can trigger panic attacks and bring about the onset of panic disorder is yet another argument for the biological bases of PD.

Animal models of anxiety and PD

The existence and validity of animal models of anxiety and panic form another argument for the biological nature of PD. These models, mainly using rodents and non-human primates, parallel human anxiety. Despite their inherent limitations, animal models of anxiety have been repeatedly proven to be useful in testing of anti-anxiety and anti-panic drugs. They are used to study neurochemical, especially central, changes in anxiety states, taking advantage of techniques such as microdialysis, single neuron recording, electro-chemical stimulation of various brain regions etc. (File, 1990).

Panic Attacks

Specific brain regions are implicated in regulation of panic anxiety

The complex nature of symptoms of PA suggests that various brain regions would be implicated. Number of techniques have been used in order to provide an explanation for panic attacks, including brain imaging, staining, electrical and chemical stimulation as well as electrical recording. Brain imaging techniques are useful tools that can provide us with information about the brain regions with higher or lower oxygen or glucose metabolism (Huang et al., 1981, Raichle et al., 1976), cerebral blood flow (Herscovitch et al., 1983), cerebral blood volume (Grubb et al., 1978), BBB permeability (Herscovitch et al., 1987) and other indices indicating activated areas (Reiman, 1990). Several studies showed apparent region-specific modifications of cerebral blood flow during panic attack (Stewart et al., 1988; Reiman et al., 1986). Alterations of the permeability of the blood-brain barrier, which is directly regulated by afferents originating in the locus ceruleus, have been linked to the development and treatment of panic disorder (Preskorn et al., 1980; Raichle, 1983).

The limbic system, especially the amygdala, has long been considered to be directly implicated in anxiety and other emotions. Amygdala receives projections from frontal cortex, association cortex, temporal lobe, olfactory system and other parts of the limbic system. It sends its afferents to frontal and prefrontal cortex, orbitofrontal cortex, hypothalamus, hippocampus as well as brain stem nuclei, such as locus ceruleus and raphй nucleus. Amygdala and its central nucleus thus communicate with many brain regions, including those that control breathing, motor function, autonomic response, release of hormones as well as processing of interoceptive and external information (Carlson, 1992). Amygdala is thus in a good position to modulate autonomic responses related to anxiety and panic because of its connections with the brain stem and the reticular formation, both of which control vegetative functions.

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