Panic + Agoraphobia Flashcards

1
Q

Define panic disorder

A

Panic disorder is an anxiety disorder characterized by recurring panic attacks, causing a series of intense episodes of extreme anxiety during panic attacks. It may also include significant behavioral changes, and ongoing worries about having other attacks.

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2
Q

Describe the diagnosis of panic disorder

A

Most people will have a panic attack once in their lifetime, however to be diagnosed with panic disorder the individual must experience recurrent, unexpected panic attacks which keep occurring.

This must be followed by at least 1month of persistent concerns and worrying about further panic attacks. This is coupled with significant non-beneficial modification of behaviour designed to avoid further attacks such as avoidance (agoraphobia is often a consequent diagnosis)

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3
Q

Define agoraphobia

A

A fear or anxiety of any place where the sufferer does not feel safe or feels trapped and is accompanied by a strong urge to escape to a safe place such as home

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4
Q

Describe the relationship between panic disorder and agoraphobia

A

The urge to escape/avoid unsafe places often is associated with the fear of having a panic attack and the consequences of an attack such as embarrassment. However, although agoraphobia is often preceded by panic attacks and disorder, it can occur independently of panic

Agoraphobic avoidance behavior is simply one of the learned consequences of having severe unexpected panic attacks.
If avoidance becomes widespread in panic disorder, panic disorder with agoraphobia is diagnosed.

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5
Q

Describe the diagnosis of agoraphobia

A

Distinct fear of situations where the individual is outside in a crowd or an open space
Situations are avoided or experienced with intense fear that they may panic etc
The individual experiences fear in at lease 2 different situation types and symptoms of anxiety or avoidance will last for 6months+
Fear causes difficulty in performing social or occupational activities and cannot be explained by the effects of other mental disorders

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6
Q

Describe prevalence

A
  • 1.5 - 3% prevalence rate over 12month for panic and 0.4% for agoraphobia
  • Both experienced more by women than men
  • Onset common in adolescence/early adulthood or during a period of stress
  • Cultural variance; Prevalence in some asian societies is low whilst in other cultures it is sometimes expressed in different symptoms such as Ataque de Nervios is an anxiety based disorder only found in Latin cultures
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7
Q

Define panic attacks

A

Discrete period of intense fear or discomfort, in which 4 (or more) of the following symptoms developed abruptly and reached a peak within 10 minutes.
Palpitations, chest tight, dizziness, unreality, hot/cold, tingling, fear lose control, fear will die, shaking, choking, sweat, blurred vision, breathless
Common in all anxiety disorders, and occur in other disorders too.

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8
Q

Rationale for looking at biological explanations

A

Due to the intense nature of physical symptoms present in panic disorder and can be used to explain the nature of panic attacks

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9
Q

Describe original biological explanation of panic

A

Metabolic studies focus on how the human body processes particular substances. Many of these studies have shown that people with panic disorder are more sensitive to certain substances than are their non-panic counterparts.

It proposes that panic attacks may be caused by a dysfunctional respiratory system. People susceptible to panic are suggested to be more sensitive to substances such as sodium lactate and CO2, which are not believed to trigger any one neurotransmitter system, are believed to provoke panic attacks by stimulating the respiratory system.

ROLE OF HYPERVENTILATION - LEY (1987)
Is a common feature of panic attacks.

Hyperventilation may be causally related to panic attacks. During hyperventilation, there is an imbalance between oxygen inhaled and CO2 exhaled, so that more CO2 is exhaled than produced, thus lowering CO2 levels in the body. In an effort to compensate for the reduction in respiratory rate caused by hyperventilation, patients experience a host of symptoms, including shortness of breath, dizziness, trembling, and palpitations. The greater the loss of CO2 as a result of hyperventilation, the stronger these secondary symptoms

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10
Q

Evidence for original biological explanations of panic

A

Evidence mostly comes from biological challenge tests which is when panic attacks are induced by administering CO2 enriched air or by encouraging hyperventilation.

Overall, findings from these studies suggest that (a) patients with PD experience a greater number of panic attacks during administration of these substances, compared with normal controls and patients with other psychiatric disorders; (b) laboratory-provoked attacks resemble naturally occurring panic attacks; and (c) drugs used to treat PD also block laboratory-provoked panic attacks from occurring.

GORMAN 1990: Two maximal inhalations of 35% CO2 proved a very powerful stimulus. All subjects,
regardless of diagnosis, experienced substantial increases in anxiety level and ventilation. This effect undoubtedly obscured putative differences between patients and controls. Baseline anxiety scores were higher for the two patient groups than for the controls

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11
Q

Evaluation for biological explanation of panic

A
  1. A more HOLISTIC APPROACH is needed to fully explain panic disorder as a purely biological explanation is inconclusive.
    – GORMAN etal 2001 Results from evidence using bio challenge tests showed that whilst physiological changes that provoke full blown attacks, it only does so in those with a history of panic even though physical changes are the same.
    Therefore, this suggests that cognitive explanations must be explored as it would appear that a significant factor for the onset of panic attacks is the way the individual interprets the changes causes rather than the physical change itself.
  2. INDIVIDUAL DIFFERENCES
    Although the theory offered here provides an explanation of the process by which the panic attack develops, it does not explain why some people are susceptible to attacks while others are not.
    - Also, although the theory can help to explain panic attacks which is a key feature of the disorder it fails to explain the other features such as the persistent fear that follows for the next few months = It is the catastrophic interpretations made by sufferers that causes panic
  3. METHODOLOGY IS FLAWED: Using bio challenge tests prove to be difficult to evaluate and judge for panic, Gorman 1990 reported that the panic/no panic evaluation was difficult to make during 35% CO2 challenge for three reasons:
    (1) the effect is very transitory,
    (2) all subjects experienced great dyspnea, and
    (3) we required that the subjects not verbally communicate their emotional reaction until 1 min after inhalation in order not to interrupt the respiratory monitoring. This difficulty is reflected in the fact that independent evaluation of six CO2 challenges in which the diagnostic blind was broken resulted in two disagreements with the attending psychiatrist about whether panic had occurred.

HOWEVER… in the broader context of laboratory-based research into panic attacks, it is worth remembering Rachman’s (1988) caution that the experimental conditions under which these panics are induced offer, by their nature, far greater control than is available in clinically occurring panics.

  1. However, high PRACTICAL IMPLICATIONS, as this theory contributes to understanding real world triggers for panic attacks. Smoking and PD have been positively associated in several epidemiological studies (Amering et al., 1999; Isensee et al., 2003; Pohl et al., 1992). Breslau and Klein (1999) and Breslau et al. (2004) found that current daily smoking increased the onset risk for panic attack and PD. Quitting smoking sharply reduces risk of panic onset.
  2. One of the major implications of bio models is that the panic attacks themselves should be a focus of treatment. This is a positive step since, even though the attacks are an important source of suffering and their alleviation may be crucial for permanent recovery, previous treatment approaches tended to neglect them. The poor prognosis of agora- phobia as opposed to simple phobias (Marks, 1970) as well as the relapses of agoraphobics occurring even after successful behaviour therapy may be due to recurring panic attacks.
  3. Challenge paradigms are ethically concerning as researchers should only use them when the effects on the patient is transitory and informed consent must be taken.
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12
Q

Describe more recent biological explanation of panic

A

KLEIN etal (1998) have demonstrated that acute hyperventilation fails to reliably produce panic attacks among panic disorder patients. They also found that air enriched with 5 percent carbon dioxide frequently induced panic attacks in panic disorder patients, which is exactly the opposite of the prediction of the hyperventilation theory.

Proposes that PD is result of a dysfunctional suffocation monitor (a “false suffocation alarm”).

Throughout the course of evolution, a highly sensitive “alarm system” has developed to detect when an organism is in danger of suffocation. High CO2 levels usually serve as an indicator that the organism is in danger of imminent suffocation, since high levels of CO2 correspond with low levels of oxygen.

Klein suggests that for PD patients their suffocation monitor becomes hypersensitive to CO2, with low levels of CO2 becoming a signal for low oxygen supply. As a result, the brain’s suffocation monitor incorrectly signals a lack of oxygen, and thus triggers a false suffocation alarm. He hypothesizes that since PD patients believe they are suffocating, (a) they experience shortness of breath and (b) they begin hyperventilating in order to keep CO2 levels well below the suffocation threshold. Therefore, rather than cause panic attacks, hyperventilation is a consequence and actually a defense against panic onset.

Klein suggests that “respiratory” panicogens such as sodium lactate, CO2, and isoproterenol elicit a false suffocation alarm (ie, a panic attack). Conversely, “neurochemical” panicogens such as yohimbine, caffeine, and mCPP produce general autonomic surges or changes similar to those created by fear, stress, or pain.

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13
Q

Describe the cognitive model of panic

A

CATASTROPHIC MISINTERPRETATION
Proposes that panic attacks occur when individuals perceive certain somatic sensations as considerably more dangerous than they truly are, and then interpret them to mean that they are about to experience sudden, imminent disaster (Negative interpretation bias that triggers anxiety which triggers panic attacks)

Clark (1988) believes that these “catastrophic misinterpretations” may arise not only from fear but also from a variety of other emotions (eg, anger) or from other stimuli (eg, caffeine, exercise).

The vicious cycle culminating in a panic attack develops when a stimulus perceived as threatening creates a feeling of apprehension. If the somatic sensations that accompany this state of apprehension are catastrophically misinterpreted, the individual experiences a further increase in apprehension, followed by elevated somatic sensations and and anxiety symptoms, until a full-blown panic attack occurs.

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14
Q

Evidence for cognitive model of panic

A
  1. Laboratory-provoked attacks may lead to similar physiological sensations in PD patients and normal controls, but only PD patients who catastrophically misinterpret these sensations will go on to develop panic attacks.
    - - ANDERSON etal (1989) found that individuals will experience panic attack when they have been told they will receive CO2 but are only given compressed air. Suggesting it is the misinterpretation that leads to the anxiety not the physical change.
  2. EHLERS+BREUER (1992) found that individual with panic disorder attend to and discriminate their bodily sensations more closely that normals. PD patients themselves report having thoughts of imminent danger during their panic attacks (eg, heart attacks, insanity) and report that these thoughts typically occur after they notice specific bodily sensation, provides convincing support for the cognitive model of panic.
  3. Additional support for Clark’s cognitive model comes from studies demonstrating that panic attacks can be alleviated with cognitive techniques, such as cognitive restructuring, which attempt to challenge and substitute catastrophic misinterpretations with rational thoughts.
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15
Q

Evaluation of cognitive model of panic

A

+ It has been argued by critics that the cognitive model does not explain why PD patients continue to misinterpret these somatic sensations despite evidence to the contrary (ie, when the catastrophic predictions do not come true).

However, since PD patients take a variety of precautions to prevent the occurrence of an attack (eg, avoid or escape situations in which they are likely to occur), it is likely that they never truly learn that their panic attacks will not lead to catastrophes no matter what safeguards they may use.

  • Problems for cognitive theory include the fact that panic attacks can occur in panic patients in the absence of detectable cata- strophic cognitions. For example, patients may experience nocturnal panic attacks. Alternatively, they may sometimes have diurnal attacks without antecedent cognitions when the cognitions should have been readily detectable
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16
Q

Describe an integrated model of panic

A

Barlow conceptualizes the initial panic attack as a “false alarm,” in which fear or panic occurs in the absence of any life-threatening stimulus, learned or unlearned. He contrasts these with “true alarms,” in which fear or panic occurs in the presence of an event that is truly dangerous or life-threatening to the organism (eg, being attacked by a gunman).

According to Barlow, individuals with PD have a genetically based biological vulnerability (ie, they are “hard-wired” to respond to the stress of negative life events with exaggerated neurobiological activity). This neurobiological overreaction or false alarm occurs because such individuals perceive life stressors as if they were truly dangerous or life-threatening (catastrophic misinterpretations).

In some of these individuals, the initial false alarm becomes associated (via classical conditioning) with the somatic sensations that accompany feelings of anxiety (eg, dizziness, palpitations). This association or conditioning leads to the development of “learned alarms,” wherein these individuals learn to become fearful of these somatic sensations because they believe they will lead to another attack.

They become increasingly anxious and apprehensive over having additional alarms or panic attacks in the future and, as a result, go on to develop PD. Their inborn predisposition to be somatically preoccupied becomes intensified as they focus even more attention on themselves, with the result being that they become even more sensitive to false alarms than they were when they had their first attack.

17
Q

Evidence for integrated model of panic

A

+ A number of studies indicate that many PD patients describe one or more negative life events as preceding their first panic attack, thus providing circumstantial evidence for the notion that the initial false alarm may result from an overreaction to a life stress.

  • However, these results must be interpreted with caution since the studies have been shown to have many methodological deficiencies. Further, other studies indicate that stress may also play a role in precipitating other psychiatric and physical disorders, suggesting that the relationship between stress and panic onset may not be unique.
18
Q

What are the different forms of treatment for panic

A
  1. Drug therapy
  2. Exposure-based therapy
  3. CBT
19
Q

Describe drug therapy treatments

A
  1. 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 — especially the tricyclic antidepressants — have anti-anxiety properties, in part, due to their sedative effects.

Antianxiety agents (benzodiazepines):

20
Q

Evaluation of drug therapy

A

+ EFFECTIVE: Two recent meta-analyses (BAKER 2002) found that selective serotonin reuptake inhibitors (SSRIs) and tricyclic antidepressants (TCAs) are equally effective in reducing panic severity and the number of attacks. In these studies, 61 percent of patients were panic-free after six to 12 weeks of treatment, compared with 41 percent of control patients.

+ LOW RELAPSE Studies also are conflicting about how
long to continue antidepressant therapy.
Studies have shown a relatively low relapse rate after six months of antidepressant therapy. Moreover, continued antidepressant therapy beyond six months does not decrease relapse rates. (Mavissakalian, 1999)
A recent studY that controlled for post-treatment therapy after CBT found no difference in relapse rates after continuing or discontinuing antidepressants. However, this study was too small to detect potentially important differences in outcomes.

  • SIDE EFFECTS
    Benzodiazepines may cause depression (Van Balkom, 1997) and are associated with adverse effects during use and after discontinuation of therapy. They also fare less well than antidepressants in other outcome measures such as global functioning. Patients with panic disorder and preexisting comorbid depression who are treated with benzodiazepines have poorer outcomes than patients taking antidepressants.
21
Q

Describe CBT for panic

A

Includes many techniques, such as applied relaxation, exposure in vivo, exposure through imagery, panic management, breathing retraining, and cognitive restructuring.

Aim: to target peoples fear of bodily sensations and their catastrophic misinterpretations and focus on challenging their beliefs in the form of corrective information and experiences designed to eliminate fault emotional responding.

Encourages patients to confront the triggers that induce arouse their anxiety. By facing the very cause of the anxiety, it is thought to help diminish the irrational fears that are causing the issues to begin with.

The therapy begins with calming breathing exercises, followed by noting the changes in physical sensations felt as soon as anxiety begins to enter the body.

Many clients are encouraged to keep journals. In other cases, therapists may try and induce feelings of anxiety so that the root of the fear can be identified

22
Q

Evaluation of CBT for panic

A

+ EFFECTIVE
1. BECK etal. examined the short- and long-term effects of a focused (12-week) course of cognitive therapy (CT) for PD. The authors also used an 8-week brief supportive psychotherapy (BST) group as a comparison group. Using both clinician ratings and patient self-ratings, they found that the focused CT accomplished significantly greater reductions in both panic symptoms and general anxiety after only 8 weeks of treatment.

  1. MITTE (2005) analyzed the efficacy of psychotherapy, pharmacological therapy, and their combination for PD/Ag in a 124-study meta-analysis: 53 pharmacological therapies, 47 psychological, and 24 combined.
    The results of behavioral treatment (BT) or CBT, compared to no-treatment, obtained high ESs in measures of avoidance/cognition/panic. The author’s conclusions are that CBT was more effective than no-treatment or placebo treatment.
  2. WESTON 2003 In the CBT trials, an average of 73 percent of treated patients were panic-free at three to four months, compared with 27 percent of control patients (number needed to treat, 2), 13 and 46 percent of treated patients remained panic-free at two years.

— Although these statistics are impressive, they represent studies in selected populations that may not reflect typical general practice patients. CBT appears to be effective over the long term (trials ranged from six months to nine years). However, these results should be interpreted with caution; the loss of patients to follow-up, unknown role of other therapies in maintaining remission, and lack of intention-to-treat analyses in many studies limit the reliability of CBT when used alone.

+ SELF HELP AVAILABLE Self-Directed CBT. If referral for formal CBT is not an option, self-directed CBT videotapes
and books have been proved effective in controlled studies (Gould, 1995). Coping with Panic: A Drug-Free Approach to Dealing with Anxiety Attacks is a widely available self-help book that has been studied in RCTs.

23
Q

General evaluation of psychopathology

A
  • Doctors do not like to talk about cure. Too many illnesses are remitting and relapsing—that is, they seem to go away only to return again at a future time. Psychiatric conditions in particular tend to be chronic. Besides, they are not as well-defined as other medical conditions. Some are clearly illnesses, similar in every way to other medical illnesses. But others seem to be only an exaggeration of the qualities of mind—mood and thought—that are present in everyone to a varying degree
  • Drugs are central to modern psychiatric practice and to much psychiatric thought about the nature and causation of mental disorders. Psychiatry has therefore become an important target for the large and powerful pharmaceutical industry. Study found that authors’ conclusions were more likely to be favourable towards an intervention where the study was fully funded by a for-profit organisation than where funding came from other sources (Kjaergard & Als-Nielson, 2002), This influence has helped to create and reinforce a narrow biological approach to the explanation and treatment of mental disorders and has led to the exclusion of alternative explanatory paradigms.