Generalized Anxiety Disorder

175.302- ABNORMAL & THERAPEUTIC PSYCHOLOGY GENERALIZED ANXIETY DISORDER: A LIFETIME CONCERN

Essay 1

Course Coordinator: Prof Dr Gillian Craven

Massey University School of Health Sciences

Department of Psychology

Palmerston North Campus

Student name: Virginia Westerberg

Date: 11 August 2010

WESTERBERG, Virginia 2 Massey University – School of Health Sciences

GENERALIZED ANXIETY DISORDER: A LIFETIME CONCERN

“Regrets over yesterday, worries over tomorrow, leave no today to live in.”

(Anonymous)

Anxiety disorders are the most common type of mental disease. Anxiety is defined as

apprehension over an anticipated event for which patients develop defence mechanisms to try

to cope with the unpleasant feelings. Anxiety disorders include phobias, panic disorder (with or

without agoraphobia), obsessive-compulsive disorder, post-traumatic stress disorder (along

with acute stress disorder) and generalized anxiety disorder (GAD) (Kring, Johnson, Davison &

Neale, 2010)

People with GAD usually expect the worst. They worry excessively about money, health, family,

school or work, even when there are no signs of trouble. They are unable to relax and often

suffer from insomnia. GAD is also associated with physical symptoms, such as fatigue, trembling,

muscle tension, headaches and irritability. REF

Leading anything resembling a normal lifestyle is not possible for people suffering from GAD as

just the thought of getting through the day provokes anxiety REFF. In the following pages, an

effort will be made to discern the diagnosis, causes, theories for maintenance and different

treatment modalities of this complex and disturbing disorder.

DIAGNOSIS

The Diagnostic and Statistical Manual of Mental Disorders (DSM-IV-TR) is the book used by

mental health professionals to establish the diagnosis of Generalized Anxiety Disorder (GAD).

The DSM-IV-TR requires at least three out of these six symptoms (one in children), some of

which must have been present regularly for more than half the days during the previous six

months:


1 .- Excessive anxiety and worry (in intensity, duration and frequency) due to an anticipated

negative outcome of future events, causing distress and interfering with a normal daily life

functioning.

2 .- Difficulty in controlling the anxiety and worry, struggling to regain control, relax, or cope

with the anxiety and worry.

3 .- The presence for most days over the previous six months of three or more (only one for

children) of the following symptoms: feeling tense or restless, becoming easily fatigue or worn-

out, concentration problems, such irritability, significant tension in muscles , difficulty with

sleep.

4.-The symptoms are not part of another mental disorder.

5.-The condition is not due to a substance or medical issue.

(American Psychiatric Association (2000). Diagnostic and Statistical Manual of Mental Disorders

(4th Ed, Text Revision). Washington DC: American Psychiatric Association.)

The most common areas of concern usually refer to conditions of daily life: relationships,

money, work, school, health, etc. Concerns may be for minor issues such as domestic activities,

the car repair or being late for an appointment (American Psychiatric Association, 1994/1995).

According to the DSM-IV-TR, children and teens with GAD are always seeking approval and tend

to worry excessively about their competence or the quality of their performance at school or

sports, even when they are not being evaluated. Also of their concern are catastrophic events

like natural disasters and wars. People with GAD can show extreme perfectionism, are unsure of

themselves and inclined to repeat their jobs due to dissatisfaction with results. (American

Psychiatric Association, 1994 / 1995).


An accurate diagnosis of GAD requires distinction between worry (or concern), fear and

obsession. Very simply put, worry is persistent intrusive mental uneasiness, fear is a feeling of

agitation due to the presence or imminence of danger and obsession is a persistent, compelling

idea or impulse. They are all associated with different degrees of arousal.

Worry or concern can be defined as a succession of thoughts and images (especially the first)

full of negative affect and that is oriented toward a possible future danger that is perceived as

uncontrollable and aversive (Rapee, 1995). This future orientation is present even when it

seems that the concern relates to a past event, due to the possible consequences derived from it.

Individuals with GAD have relatively constant worries and very rarely can they shelve an issue

of concern at the emergence of a new concern (Deffenbacher, 1997). It is quite possible that the

concerns are closely related to intolerance of uncertainty (Dugas et al., 1998). Concern is usually

seen as caring, a socially praised attitude which, if in excess, can become intrusive and

maladaptive (Craske, Barlow & O'Leary, 1992, pp. 1-7).

These concerns are associated with hypervigilance or excessive attention to threatening stimuli

and a sense of uncontrollability of them. On the other hand, Butler (1994) indicates that clinical

observation shows that the focus of concerns of patients with GAD changes repeatedly, but

there is great individual variability in the speed with which these changes occur.

Dugas et al., (1998) have classified concerns as related to current issues (to meet the deadlines

at work / school, interpersonal conflicts) or to improbable future events (death of son in an

accident). Moreover, Ladouceur et al., (2000) identified two types of concerns: a) about

modifiable situations (treatable through problem solving) and b) about non-modifiable


situations (which often do not exist yet). The latter authors suggest that each type of concern

requires a different intervention.

Associated conditions found during the course of GAD should also be noted and taken into

account in the diagnosis. Patients with GAD often present additional disorders such as major

depressive disorder, dysthymia, panic disorder (with or without agoraphobia), social phobia,

specific phobias, alcohol abuse or dependence of sedative, hypnotic or anxiolytic drugs. Physical

disorders that are also frequent are those associated with stress (e.g., irritable bowel syndrome,

headaches, essential hypertension, ulcers, cardiovascular disorders, diabetes, insomnia and

even cancer) (American Psychiatric Association, 1994/1995; Laberge & Gosselin, 2003; Rapee,

1995). Children and adolescents with GAD, compared to those with other anxiety disorders,

show more comorbid anxiety disorders. Other common associated conditions, apart from a

range of depressive disorders and phobias, are separation anxiety disorder, panic disorder and

attention deficit hyperactivity disorder (Sandin, 1997).

AGE OF ONSET AND COURSE

Most patients with GAD say they have been nervous throughout life, that is why some authors

have considered GAD as an anxious personality disorder (Rapee, 1995). Half of patients with

GAD report that their disorder began in childhood and adolescence, although onset after the age

of twenty is not uncommon. Symptoms of GAD tend to develop at the beginning of adulthood

coinciding with life events such as the accumulation of responsibilities, childbirth, labour

difficulties and health problems (Gosselin and Laberge, 2003).

The course of the disorder is chronic, albeit with fluctuations dependent on the presence or

absence of periods of stress (American Psychiatric Association, 1994/1995). In severely ill

patients with long-term GAD (M = 20 years) the probability of full remission after 1, 2 and 5


years was only 15%, 25% and 38% respectively, despite having received pharmacotherapy and

some psychological treatment (psychodynamic, behavioural, cognitive-behavioural). Of the

patients, 27% relapsed within a period of three years (Yonkers et al. 1996, 2000). Referrals

were less likely in patients who had poor family or marital relationships, personality disorders,

group B or C or worse overall satisfaction with their lives (Rapee, 1995).

Compared with other patients with anxiety disorders, it is less common that patients with GAD

seek treatment, perhaps because this disorder causes just moderate disturbance or because

people accept it as a way of being. Additionally, patients with GAD may not be seen in the

psychological consultation because they will already have been seen by their GP complaining of

physical symptoms for which drugs are usually prescribed (Craske, Rapee & Barlow, 1992).

PREVALENCE

In an epidemiological study of 10,641 Australians (Hunt, Issakidis & Andrews, 2002), GAD was

found with a monthly and annual prevalence of 2.8% and 3.6% respectively. The annual

prevalence of GAD was 1.0% (0.5% in males and 1.3% in women) and the lifelong prevalence

2.8% (2.0% in males and 3.6% in women).

The prevalence of GAD in childhood appears to be 3-4% according to studies cited by Eisen and

Silverman (1998). In adolescents, GAD is believed to be the most common anxiety disorder, the

numbers have fluctuated between 3.7% and 14% and the modal value can hover around 7%

(Wicks, Nelson and Israel, 1997). About 60-70% of people with GAD are women. Hormonal,

environmental and specific life events (maternity) may in part account for the differences.

(Dugas and Ladouceur, 1997, Kessler et al. 1994; Wittchen et al. 1994).


GAD is also more common in those over 24 and under 55 years of age, and in the separated /

widowed / divorced, the unemployed and housewives (Hunt, Issakidis and Andrews, 2002;

Wittchen et al., 1994). In contrast, the level of education, religion and rural / urban are not

predictors. Although the trait of anxiety runs in families, it is not yet clear that GAD is more

frequent in relatives of patients with GAD than in relatives of control people, although a few

studies suggest so (Hettema, Neale and Kendler, 2001) .

AETIOLOGY AND MAINTENANCE

There are several factors that account for the aetiology of GAD: genetic, neurobiological,

environmental, psychological (personality and cognitive) and integrative. These factors may

predispose to GAD but not all individuals will develop it as some will have learned how to

confront their tendency. Maintenance of the symptoms lies mainly on the psychological aspects

of the condition.

Genetic factors

Studies carried out by the NARSAD (National Alliance for Research on Schizophrenia and

Depression) (Archives of General Psychiatry, 2008) have shown that an area of chromosome 1

is associated with an anxious temperament, particularly the gene that encodes the RGS2 protein,

which mediates the activity of neurotransmitter receptors that are also the target of many

antidepressant and antipsychotic drugs.

Functional MRI brain imaging was done to participants in NARSAD studies while viewing faces

expressing a series of emotions. It showed an increased activity in the amygdala, a gray matter

nucleus located in the anterior portion of the temporal lobe, which is associated with assigning

emotional significance to stimuli (Kring, Johnson, Davison & Neale, 2010). Participants with the

inhibition / introversion-associated alleles showed increase activity of the amygdala and the


insula, another anxiety-related brain region. Whether these RGS2 variants are associated with

particular disorders and how they act on a cellular level remains to be investigated (Archives of

General Psychiatry, Vol 65 (No. 3), Mar 2008). Although the genetic load in anxiety disorders

has been documented, studies are not conclusive for patients with GAD (Hettema, Neale and

Kendler, 2001).

Neurobiological factors

Neurobiological hypersensitivity to stress may also be genetically determined. This biological

vulnerability can interact with a psychological vulnerability (feeling that threatening events are

unpredictable and / or uncontrollable based on early developmental experiences), so that upon

the occurrence of stressful events or problematic, the person may respond with concern and

anxiety; this response will be moderated by factors such as coping skills and social support

(Barlow, 1988, 2002).

What all anxiety disorders have in common is a state of increased arousal (Barbee, 1998)

known as “fight-or-flight” response, also referred to as the acute stress response. When a

fearful or threatening event is perceived, humans react innately to survive: they either are ready

for battle or run away. The result is a sudden increase in heart and respiratory rate, blood

pressure, sweating, metabolism, and muscle tension. Enhanced cardiac output and accelerated

metabolism are essential for mobilizing fast action and to reduce reaction time to threats. The

string of changes start in a nucleus in the brainstem called the locus ceruleus, which is the origin

of most norepinephrine (noradrenaline) pathways in the brain, connecting with the cerebral

cortex, limbic system and the spinal cord.

When a stimulus, feeling or thought is perceived as a threat, the discharge of the locus ceruleus

activates the sympathetic division of the autonomic nervous system (Thase & Howland, 1995)


leading to the release of norepinephrine from nerve endings acting on the heart, blood vessels,

respiratory centres, and other sites (gastrointestinal tract, skin, kidneys, etc.).

In the 1980’s, the prevailing view was that excess discharge of the locus ceruleus with the acute

stress response was a major contributor to the aetiology of anxiety (Coplan & Lydiard, 1998).

Yet over the past decade, the limitations of the acute stress response as a model for

understanding anxiety, and specifically GAD, have become more apparent. The first and most

obvious limitation is that the acute stress response relates to arousal rather than anxiety.

Anxiety differs from arousal in several ways (Barlow, 1988; Nutt et al., 1998).

Firstly, with anxiety the concern about the stressor is out of proportion to the realistic threat.

Secondly, anxiety is often associated with elaborate mental and behavioural activities designed

to avoid the unpleasant symptoms of a full-blown anxiety attack. Thirdly, anxiety is much longer

lived than arousal. Finally, anxiety can occur without exposure to an external stressor. In any

case, arousal is mild to moderate in patients with GAD compared with those suffering from

other anxiety disorders, like phobias.

Another neurobiological cause of anxiety is neurotransmitter imbalance. Serotonin,

norepinephrine, gamma-aminobutyric acid (GABA), corticotropin-releasing hormone (CRH) and

cholecystokinin (Coplan & Lydiard 1998; Rush et al., 1998) are the five most important ones.

Homeostasis between these neurotransmitters means that changes in one neurotransmitter

elicit changes in another due to feedback mechanisms. Serotonin and GABA are inhibitory

neurotransmitters that quiet the stress response (Rush et al., 1998). All of these

neurotransmitters have become important targets for today´s therapeutic agents.


Psychological factors, Personality and Cognitive Traits.

The main psychological theories about the genesis of anxiety are: psychoanalytic and

psychodynamic, behavioural, and cognitive (Thorn et al., 1999). Psychodynamic theories have

focused on symptoms as an expression of underlying conflicts (Rush et al., 1998; Thorn et al.,

1999). Although there are no empirical studies to support these psychodynamic theories, they

are amenable to scientific study (Kandel, 1999) and some therapists find them useful. From the

psychodynamic perspective, anxiety usually reflects more basic, unresolved conflicts in intimate

relationships or expression of anger.

Recent behavioural theories have emphasized the importance of two types of learning: classical

conditioning (originally developed by Pavlov) and vicarious or observational learning

(originally developed by Bandura). In classical conditioning, a neutral stimulus acquires the

ability to elicit a fear response after repeated pairings with a frightening (unconditioned)

stimulus. In vicarious learning, fearful behaviour is acquired by observing others’ reactions to

fear-inducing stimuli (Thorn et al., 1999). In the case of GAD, unpredictable positive and

negative reinforcement is seen as leading to anxiety, mainly because the person is unsure about

whether avoidance behaviours are effective.

Cognitive factors, especially the way patients interpret or think about stressful events, play a

critical role in the aetiology of GAD (Barlow et al., 1996; Thorn et al., 1999). A decisive factor is

the individual’s perception, which can intensify or dampen the response. One of the most salient

negative cognitions in GAD is the sense of uncontrollability. It is typified by a state of

helplessness due to a perceived inability to predict, control, or obtain desired results (Barlow et

al., 1996). Negative cognitions are frequently found in individuals with GAD (Ingram et al.,

1998). Many modern psychological models of anxiety incorporate the role of individual

vulnerability, which includes both genetic (Smoller & Tsuang, 1998) and acquired (Coplan et al.,


1997) predispositions. There is evidence that women may ruminate more about distressing life

events compared with men, suggesting that a cognitive risk factor may predispose them to

higher rates of anxiety and depression (Nolen-Hoeksema et al., in press).

Borkovec (1994) distinguished two components of psychological vulnerability having to do with

cognitive factors related to GAD: the overall perception of threat (hypervigilance or world view

as dangerous) and feeling unable to cope with threatening events (lack of control). This

vulnerability has arisen from the experience of certain experiences of trauma and rejection by

parents. Compared to subjects without GAD, GAD similar subjects have reported a higher

frequency of traumatic events in the past both in general and for specific types of trauma

(illness / injury / death, assault / sexual, emotional events with family and friends, etc.). Other

historical factors associated with GAD are the loss of a parent before age 16, alcoholic parent,

verbal abuse and lack of care / affection during childhood. All these variables may predispose to

GAD, although other interpretations exist: the GAD could be prior to trauma, chronic anxiety

may influence the perception or reaction to trauma (although the influence may be

bidirectional) or in the subsequent report the same, and differences in traumatic events cannot

be seen in prospective studies.

People with GAD often exhibit personality traits such as perfectionism, dependence and lack of

assertiveness (Rapee, 1995), which may have been favoured by being raised by overprotective,

demanding and / or anxious parents. These personality characteristics may contribute to the

lack of skills to handle various difficult situations or difficulty to apply those skills. Dugas and

Ladouceur (1997) noted that, in general, patients with GAD do not lack knowledge on how to

solve problems, but fail in the orientation towards the problem (not able to recognize the

problems or see problems where none exist, inappropriate approach to them, value them as

threats and are frustrated and disturbed to find they don’t resolve, not believing in one's ability


to solve them, not spending enough time and effort solving them and keeping a pessimistic view

on the results, etc. In general, their reactions show affective, cognitive and / or behavioural

inadequacy as mentioned in Ladouceur et al., (1998).

Individuals with GAD learn to be hypervigilant to uncover potential threats. It seems that the

bias of attention is accompanied by an explicit memory bias towards threatening information,

suggesting an avoidance of cognitive processing of this information. However, the threatening

information is encrypted even after detection avoidance, as suggested by the implicit memory

tests (people with GAD recall more words with threatening meaning) (Borkovec, 1994; Rapee,

1995).

Along with the attentional bias, people with GAD have a lower threshold for perceiving

ambiguity and tend to interpret ambiguous information as threatening (a noise at night means a

thief, hearing that there was a car accident suggests that a relative is involved) (Rapee, 1995).

Moreover, Ladouceur, Talbot, and Dugas (1997) have highlighted intolerance of uncertainty and

emotional arousal as key phenomena in anxiety disorders in general and GAD in particular.

Intolerance of uncertainty is considered the dysfunctional way in which the person collecting

the information in uncertain or ambiguous situations responds with a series of reactions:

cognitive, emotional and behavioural. More specifically, intolerance of uncertainty is the general

tendency of a person to consider unacceptable that a negative event may occur, although the

probability of its occurrence may be small (Buhr Dugas, 2002).

lntolerance of uncertainty contributes to the development and maintenance of the concerns

both directly (more attention to ambiguous events, which are perceived as threatening to the

time that exaggerates the likelihood of the threat) as indirectly, by interfering with the


application of skills troubleshooting (higher levels of emotional arousal, decreased self-

confidence to solve problems, perception difficulties when there is really no problems, not being

able to decide because it is not a perfect solution, require more data or information before make

a decision).

Prior cognitive biases (attention bias toward threat, interpretation of ambiguous information as

threatening) with other factors such as intolerance to uncertainty, negative orientation to

problems (e.g., perception of little control over issues which are seen as threatening, and the

very process of problem solving) and the possible deficits in solving problems give rise to

concerns, which involve an overestimation of the likelihood and cost of the threats zas . The

concerns are also compounded by the occurrence of stressful life events (Borkovec, 1994, Dugas

and Ladouceur, 1997; Rapee, 1995).

The belief that worries are useful contribute to their perpetuation (e.g., a superstitious

coincidence between worry and lack of negative results. Patients with GAD report beliefs that

either focus on controlling the external environment and involve probably delayed negative

reinforcement concerns or focus on controlling one's emotions and behaviours and provide

probably a more immediate reinforcement (Borkovec, 1994, Dugas and Koerner, 2005).

Concerns generate anxiety, which patients try to control with certain behaviours. Brown,

O'Leary, and Barlow (2001) defined behaviours of concern as active or passive avoidance of

certain activities to reduce or prevent anxiety and the supposed anticipated dangers. Examples

are frequently calling loved ones or else hospitals when they are delayed, often consulting

doctors for symptoms noted in themselves or family members, frequently cleaning the house in

case someone comes to visit unexpectedly, refusing to read obituaries or bad news in the


newspaper or talk about them, etc. These behaviours of concern help maintain worries and

interpretations of threat.

On the other hand, Wells (1995, 1997) pointed out that over time patients develop negative

beliefs about worry because they start becoming more uncontrollable and disruptive) and /or

because of fear to become insane because of his permanent worrying. These negative beliefs

stimulate what Wells (1997) termed Type 2 worries or concerns about cognition itself, in

particular concerns about the occurrence of worry (metaworries). These metaworries are more

frequent in patients with GAD than in non-anxious subjects (Davis & Valentiner, 200, cited in

Gosselin and Laberge, 2003) and should be distinguished from Type 1 worries or concerns

about external events and non-cognitive internal events (physical symptoms).

Integrative Perspective:

Many clinicians believe that GAD is very likely caused by a combination of biological,

psychological and environmental (family, social) factors. For example, one person may have a

genetic predisposition to develop GAD but it never becomes a problem because the person

learns coping strategies and never experiences intense distress. However, another person with

the same disposition may develop GAD due to a strong environmental influence from a parent

or because he experienced a traumatic event as a young person.

QUESTIONNAIRES AND SCALES OF ASSESSMENT

There are questionnaires and rating scales designed to assess general anxiety, worry, the key

variables associated with GAD, and situations arising individual levels of anxiety. Unfortunately,

the questionnaires of anxiety did not tend to discriminate patients with GAD patients with other

anxiety disorders (excluding specific phobias).


A good set of questionnaires could include one of anxiety, Individualized Situation Hierarchy

Associated with Anxiety Inventory Pennsylvania State Concern, the Scale of intolerance of

uncertainty, the scale of the Consequences of Worry (or “why should I care?”) and the Inventory

of Social Problem Solving.

TREATMENT

Anxiety disorders are treated with psychotherapy or pharmacotherapy, either singly or in

combination (Barlow & Lehman, 1996; March et al., 1997; American Psychiatric Association,

1998; Kent et al., 1998).

1.- PSYCHOLOGICAL TREATMENT

GAD is, to varying degrees, responsive to psychotherapy. Acute and more severe and persistent

symptoms may require additional pharmacotherapy (American Psychiatric Association, 1998).

During the past several decades, cognitive behavioural therapy (CBT) has been emphasized,

even imposed, as the arguably single, most effective, longer-lasting, non-pharmaceutical relief of

anxiety symptoms (Barlow & Lehman, 1996).

The hallmarks of CBT consist of evaluating apparent cause and effect relationships between

thoughts, feelings, and behaviours, as well as implementing relatively straightforward strategies

to lessen symptoms and reduce avoidant behaviour (Barlow, 1988). Other forms of

psychological treatment are: psychodynamic therapy, supportive therapy and self-assessment,

and neuromodulation. The latest developments in psychotherapy for GAD are discussed at the

end of this section.


1. Cognitive Behavioural Therapy (CBT)

First presented separately as behaviour modification (Skinner, 1953) and cognitive therapy

(Beck 1979), cognitive-behavioural therapy (CBT) incorporates elements of both behaviour

therapy (BT) and cognitive therapy (CT). CBT helps identify irrational thoughts that cause

anxiety. The patient faces his negative automatic thoughts and dysfunctional underlying beliefs

through "hypothesis testing" with the use of behavioural tasks between sessions while keeping

a diary, which will be used to test the validity of the beliefs and of the skill training sessions.

Examples of CBT interventions developed for the treatment of anxiety disorders include

training for the treatment of anxiety (Suinn 1977), cognitive restructuring, situational exposure

and self-desensitisation (Borkovec, 1988).

Modern treatments for anxiety disorders often include relaxation techniques such as stimulus

control, the alternative self-statements, images and soothing relaxation with meditation, which

can also be applied as isolated interventions (Ost 1987). For this reason, although it is

recognized that the therapy / relaxation training (RT) is sometimes used for comparison of

control and attention placebo in trials of psychological therapy, this technique should be seen as

an active intervention of CBT, in accordance with previous reviews (Borkovec, 2001).

2. Psychodynamic Therapy (PT)

Based on psychoanalytic theory (Freud 1949), psychodynamic therapy (PT) uses the

therapeutic relationship to explore and resolve the unconscious conflict, with the development

of self-knowledge and character change limited as therapeutic targets and the relief of

symptoms as a indirect outcome. More modern models of psychodynamic therapy have been

developed by Malan 1963, 1972 and Mann Balint 1973. This approach is not useful in the

treatment of GAD.


3. Supportive Therapy (ST)

Supportive therapy (ST) can be divided in active or inactive interventions:

Active Supportive Therapy

Included in this category are psychological therapies supported by humanistic principles:

a) Roger’s person-centered therapy (Rogers, 1951) is considered experimental in approach and

the therapist uses empathy, acceptance and authenticity within the therapeutic relationship to

facilitate customer self-awareness and self-determination. In recent years, researchers have

developed versions of the original manuals regarding the person-centered therapy, for use as a

control procedure in trials of psychological therapy, and include non-directive therapy

(Svartberg, 1998), non-directive counselling (Blowers, 1987) and listening to support

(Borkovec, 2001).

b) Gestalt therapy (Perls, 1976) increases individual self-awareness and perception of time,

especially in relations with others and the environment.

c) Transactional analysis (Transactional Analysis) (Berne 1961) is based on an understanding of

the interactions (transactions) between patient and therapist, and between the patient and the

others in his environment.

d) Counselling is a psychological therapy that arises predominantly from humanistic or

integrative approaches and is viewed as an active supportive therapy.

Inactive Supportive Therapy

These are inactive interventions used in trials as a control for attention-placebo groups, without

a psychotherapeutic framework defined or appropriate supporting references.


4.- Self Registration

Self-registration is the use of observation and record of the patient’s own behaviour for the

modification of the latter. It may be seen as a form of treatment based on self-awareness or

Mindfulness (Kabat-Zinn, 2010).

Several models of self-registration can be used for the assessment of GAD. In one of them, the

patient, at the end of the day, grades himself according to his average level of anxiety in a scale

from 0-8, his highest level of anxiety, his average level of depression, his average level of

positive affect and the percentage of days (0-100% ) his condition was present (Brown, O'Leary,

and Barlow, 2001). In another more immediate self-registration, each time the patient feels

worried or anxious he is to record the precipitating factors (situational, cognitive or emotional),

level of anxiety and worry, thoughts or behaviours engaged and methods employed to reduce

the worry or anxiety. Butler (1994) pointed out other interesting aspects to be evaluated:

number of daily setbacks, degree of discomfort associated with worry and the level of

interference in daily life skills in terms of concentration, decision making, sleep, relaxation and

pleasure, etc., whichever applies in each patient.

5.- Latest developments in psychotherapy

Recently developed promising interventions for the treatment of GAD in adults are those of

Brown, O'Leary, and Barlow (2001), the Dugas group (Dugas and Koerner, 2005) and

neuromodulation (Lozano &Mayberg, 2008). Kendall’s treatment for children deserves a special

mention here.

BROWN, O'LEARY AND BARLOW TREATMENT

Brown, O'Leary, and Barlow (1993, 2001) developed a combination treatment for GAD that

includes conceptualization of the problem and justification for treatment, relaxation training,


cognitive restructuring, exposure to the concern, preventing the conduct of concern, time

management and problem solving.

DUGAS GROUP TREATMENT

The Dugas group (Dugas and Koerner, 2005, Dugas and Ladouceur, 1997) proposed another

type of intervention for GAD that includes not only the conceptualization of the problem and

rationale for treatment, training to realize their concerns and type, re-evaluation of the

usefulness of each specific concerns, specific interventions for concern (training in problem

solving, exposure, cognitive disability) and relapse prevention.

NEUROMODULATION

An estimated 25% of patients with GAD are partially or totally resistant to the medical

treatment. Those who suffer from treatment-resistant anxiety were left with no alternatives.

Thus, there was a need to develop alternative treatments for these patients. The use of

neuromodulation through electrical or auditory stimuly for treating neurological disease,

including GAD and such disorders as Parkinson's disease, essential tremor, dystonia, and

chronic pain, has been widely discussed in the literature (Lozano &Mayberg, 2008). It has been

recognized that neuromodulation holds significant advantages over not only medical treatment

but over alternative surgical interventions since lesioning irreversibly destroys the nervous

system tissue. Thus, in many instances, the preferred therapy may be an attempt to modulate

neuronal activity in order to harmonize the firing sequence of the target neurons.

KENDALL’S TREATMENT

As regards children, Kendall (1994, Kendall et al. 1997) has proposed a cognitive-behavioural

treatment (program FEAR: False Emotions Appearing Real) led to anxiety disorders in general,

although it has been applied especially disorder in children hyperansiety syndrome (the former

name for the GAD when the DSM-III-R distinction between children and adults on this). This

treatment has been shown clinically and statistically superior to the waiting list for children


with various anxiety disorders (generalized, separation or social), the first being the largest

group.

Moreover, the FRIENDS program used by Barrett and colleagues (an adaptation of Kendall's

FEAR program) has demonstrated social validity, because its users show a high satisfaction with

it and most would recommend it to others. Interestingly, children scored more highly cognitive

strategies and gradual exposure adolescents (Barrett, Shortt and Wescombe, 2001). The

FRIENDS program, besides teaching anxiety management techniques to the child, reduces

conflict and increases cooperation in the family.

2.- MEDICAL TREATMENT

The current trend for the treatment of GAD are venlafaxine and paroxetine, although the most

common medical treatment is the combination of benzodiazepines and azopyrines. Recent

investigations have shown promising results using tricyclic antidepressants, SSRIs and SNRIs

(Roy-Byrne & Cowley, 2002).

Benzodiazepines (diazepam, lorazepam, alprazolam) are better than placebo in the short term.

They relieve somatic symptoms more than psychological symptoms though, and they are not

recommended as long-term treatment due to tolerance, dependence, and side effects like

memory loss (inhibiting the learning of stress-coping strategies of cognitive behavioural

treatment), decreased alertness, enhancement of the effects of alcohol, etc. Moreover, the

percentage of relapses after discontinuation of benzodiazepines is high (63-81%). GAD and

depression often coexist and benzodiazepines are frequently prescribed in these cases. But

benzodiazepines may both cause and aggravate depression, possibly by reducing the brain's

output of neurotransmitters such as serotonin and norepinephrine and benzodiazepines have

been shown to precipitate suicidal tendencies in some of these patients.


Benzodiazepines are useful for acute anxiety reactions, because they are very fast acting, and

can be used episodically or intermittently as adjunctive therapy in acute exacerbations of

generalized anxiety or sleep disturbances when starting treatment with antidepressants. The

use of benzodiazepine for anxiolytics purposes should be limited to a maximum of three

months, including the month of gradual withdrawal (Roy-Byrne & Cowley, 2002).

Buspirone (20-60 mg / day), an azopyrine compound, is a relatively selective 5- HT1A partial

agonist (Stahl, 1996). It appears to be as effective as benzodiazepines, but has not always been

superior to placebo. It is not as fast acting as benzodiazepines (2-4 weeks) but has fewer side

effects (dizziness, headache, nausea, generally weak) and does not seem to cause sedation or

dependence. On the other hand, it is not effective against comorbid disorders and it requires

multiple daily doses. Azopyrines are more efficient with cognitive symptoms than somatic

symptoms. Combination with benzodiazepines can have a synergistic effect (Roy-Byrne &

Cowley, 2002).

Tricyclic antidepressants (imipramine) are slower acting (3-4 weeks) and not as well tolerated

as benzodiazepines and azopyrines, leading to more dropouts from treatment due to side effects

(overstimulation, restlessness, weight gain, sexual dysfunction, impair cardiac function) and are

dangerous in the hands of suicidal patients (Roy-Byrne & Cowley, 2002).

Within the selective inhibitors of serotonin reuptake inhibitors (SSRIs), sertraline was more

effective than placebo in a study with children and adolescents (5-17 years) (Rynn, Siqueland

and Rickels, 2001). Sertraline and paroxetine appear to be equally effective. The results of a

study suggest that SSRIs (paroxetine or citalopram) not only reduce anxiety, but also

interpretation of ambiguous information as threatening.


Venlafaxine extended release (a serotonin and norepinephrine reuptake inhibitor)

improvements occur not only at symptomatic level, but also at social adjustment level. Side

effects of venlafaxine extended release are mild (nausea, drowsiness, dry mouth, dizziness,

sweating, constipation, anorexia and sexual dysfunction) and it is well tolerated (Roy-Byrne &

Cowley, 2002).

Other drugs that have been investigated in a study are enciprazine, hydroxyzine, opipramol, DN-

2327-a derivative of isoindolin-and pregabalin, a structural analogue of gamma-aminobutyric

acid-(more effective than placebo), alpidem (as effective as benzodiazepines), nefazodone, and

milnacipram, a reuptake inhibitor of serotonin and norepinephrine.

The effectiveness of pharmacological treatment in GAD has not been established in patients

with comorbid disorders, especially major depression.

Another important aspect to note is that positive response to placebo in the treatment of GAD is

very high, 30 to 40%. This supports the importance of psychological factors in the genesis of

this condition (Schweizer and Rickels, 1997).

In the case of children, Kendall et al., (1997) cite several studies indicating that fluoxetine is the

only drug that has proven effective in this group.

Given its relative efficacy, tolerability and safety, and its usefulness when affective disorders or

comorbid anxiety, venlafaxine and selective inhibitors of serotonin reuptake (particularly

paroxetine) are medications that are recommended for continued drug treatment of GAD in

adults. Kaplan, Sadock and Grebber (1994/1996) suggest that drug treatment may be carried

out over a lifetime, and that 25% of patients relapse within the first month after stopping


treatment and 60-80% in the following year. However, they claim it is a mistake to continue

treatment with benzodiazepines indefinitely.

3.- PSYCHOLOGICAL vs MEDICAL TREATMENT

Some studies have compared the effectiveness of psychological and pharmacological

treatments. Lindsay et al., (1987) found that CBT was equal to lorazepam in the aftercare, but

did not get that the medicated patients leave the medication at 3 months follow-up. Power et al.,

(1989, quoted in Power et al. 1990) found that CBT was more effective than diazepam (low

dose) and placebo at posttreatment and follow-up at 12 months.

Gould et al., (1997) conducted a meta-analysis that compared the effectiveness of cognitive-

behavioural and pharmacological approaches. Both were clearly effective and not different

between them in measures of anxiety. The first achieved better effects on measures of

depression and maintenance of the results in follow-up at 6 months, while in the latter there

was a noticeable loss of efficiency due to discontinuation of medication. In a subsequent meta-

analysis, Mitte (2005) found no differences between cognitive-behavioural and pharmacological

considering only studies that directly compared both types of therapy.

A few studies have compared psychological treatment, medication and their combination.

Power et al., (1990) investigated in patients with GAD recent five treatments over 10 weeks:

CBT alone or combined with diazepam or combined with placebo, diazepam and placebo.

Results at post-treatment and follow-up at 6 months showed superiority over placebo with CBT

treatments, especially when applied alone or in combination with diazepam. The latter was no

more effective than placebo, but was given a fixed dose and low.

The tentative conclusions to be drawn from previous work is that acute or serious GAD cases

should first be approached with medication and then followed by psychotherapy. Gradual

withdrawal of drugs over 3-6months should ensue and that the psychotherapeutical


intervention leads to better health outcomes in the medium and long term management of

patients with GAD.

REFERENCES

As per paper requirements, references were sent in a separate attachment for word count

purposes.

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Generalized Anxiety Disorder

Health & Medicine