Anxiety Disorders: A Pocket Guide For Primary Care (Current Clinical Practice)

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Some investigators believe that the essential missing component in early childhood is the unprovoked change in bodily sensations, rather than the ability to impose a catastrophic interpretation. Unlike the other anxiety disorders, a diagnosis of posttraumatic stress disorder PTSD rests on a clearer causal sequence in which a person is first exposed to a traumatic event, feels frightened because of the threat to personal integrity, and then develops the disorder. Patients with PTSD present three kinds of symptoms.

First, the patient must suffer from episodes of reexperiencing the traumatic event, which can include recollections of the event manifested in flashbacks or recurring dreams.

Panic disorder

Second, patients must attempt to avoid any event or place associated with the trauma, and the avoidance is accompanied by feelings of numbness or reduced responsivity. Finally, PTSD patients must experience signs of increased physiological arousal, especially difficulty falling asleep, increased irritability, or exaggerated startle. As with panic disorder, there is some debate over whether children exposed to trauma manifest all three symptoms. Children are likely to display separation anxiety disorder following a traumatic event.

Accurate estimates of the prevalence of DSM anxiety disorders are only available for children older than 8 years of age because studies of younger children have failed to have population-based samples and clear diagnostic criteria these studies often use symptom scales rather than diagnostic indices or have failed both requirements. The best estimates of the prevalence of anxiety disorders in preschool children, based on a primary care clinic sample Lavigne et al.

The prevalence of any anxiety disorder increases with the duration of time over which the symptom's presence is counted. Thus 3-month estimates range from 2. By contrast, instruments designed specifically for children yield lower prevalence rates. Thus caution should be exercised when adult diagnostic instruments are used with children.

The relation between the diagnosis and everyday functioning remains a focus of controversy. The prevalence of anxiety disorders varies according to whether disability is or is not part of the definition. If a child must meet the criteria for a diagnostically relevant symptom as well as impairment in everyday functioning, the prevalence of a diagnosis is reduced by two-thirds.

The prevalence of simple phobia was affected most severely; the prevalence fell from Thus, all estimates of the frequency of the anxiety disorders depend in a serious way on the source of evidence and the criteria adopted. Most investigators report that girls are more likely than boys to have an anxiety disorder.

For example, more girls than boys between ages 9 and 16 years participating in the Great Smoky Mountains Study had an anxiety disorder Three studies revealed more phobias in girls, two reported more panic disorder and agoraphobia in girls, and only one study found more separation anxiety disorder and OAD in girls than in boys.

One confound was the fact that the child's age is often correlated with the time frame used to estimate symptoms. Investigators who used 3-month prevalence rates reported the lowest prevalence but studied the youngest subjects. By contrast, investigators using month estimates had the highest prevalence but worked with the oldest children. In the Great Smoky Mountains Study the prevalence of separation anxiety decreased with age, whereas social phobia, agoraphobia, and panic disorder increased with age. It is difficult to draw conclusions about gender differences in the fears, worries, and anxieties of clinic-referred samples either clinically anxious samples or other types of clinical samples given the limited amount of research that has been conducted.

Rates of GAD and specific phobias remain constant across childhood and adolescence. Although girls are more likely than boys to have an anxiety disorder, the gender difference is not as marked in the general population as it is in clinical samples, perhaps because boys are less likely to be referred for treatment. Numerous studies have demonstrated that girls who mature earlier than their peers exhibit higher rates of anxiety symptoms and disorders e.

Comorbidity among the anxiety disorders has been a problem for nosology, epidemiology, diagnosis, and treatment. A review by Costello et al. The criteria for GAD are permissive, hence a child could receive this diagnosis if he or she displayed only one of the six critical symptoms restlessness, fatigue, difficulty concentrating, irritability, muscle tension, or sleep disturbance. The GAD symptoms are different from those that define OAD worry about the past or future, concern about one's competence, need for reassurance, somatic symptoms, excessive self-consciousness, and muscle tension.

Further, the new criteria for GAD resemble those used to diagnose major depressive episodes; examination of the overlap between OAD and GAD should take into account the possibility of a correlation with depression. Most published studies confirm comorbidities among the three phobias: However, none had any association with PTSD after investigators controlled for other anxious comorbidities. There is no significant concurrent comorbidity between panic disorder and separation anxiety, but this tendency does not rule out the possibility of sequential comorbidity.

There is little association between separation anxiety and either phobias or OAD. Comorbidity between any one anxiety disorder on the one hand, and ADHD, conduct disorder, depression, or substance abuse disorder on the other, reveals the highest level of comorbidity with depression, with a median odds ratio of 8.

Coexisting Depression and Anxiety: Classification and Treatment : Acta Medica Martiniana

There is also a sequential link between early anxiety and later depression Costello et al. It is not clear, however, whether depression or anxiety increases the subsequent risk for the complementary disorder or whether the natural sequence is from an initial anxiety disorder to the later development of depression. These confidence intervals imply a significant degree of comorbidity.

Although the bivariate odds ratios that involve substance use or abuse were significant in some studies, an association between anxiety and substance abuse disappeared when comorbidity between anxiety and other psychiatric disorders was controlled Costello et al. Although there is little concurrent comorbidity for anxiety and substance abuse Weissman et al. Kaplow, Curran, Angold, and Costello reported that children with separation anxiety were less likely than others to begin drinking alcohol, and if they did, they did so at a later age than that of most youth.

But children with GAD were more likely to begin drinking and abuse alcohol earlier in adolescence. The evidence does not permit a confident reply to the question of whether anxiety disorders in preschool children are precursors of similar disorders in adolescents. The Great Smoky Mountains Study revealed that specific phobias, GAD, separation anxiety, and social phobia all appeared around the time the child began school, while agoraphobia, OAD, and OCD appeared several years later, usually at 9 to 11 years of age Costello et al.

Separation anxiety and phobic disorders are seen in early childhood but become rare by adolescence. However, panic disorder and agoraphobia have the opposite developmental profile; they are rare in childhood and increase in adolescence. We do not yet know whether some adolescent disorders are later manifestations of an underlying syndrome that was displayed earlier or whether they represent new forms of psychiatric illness.

An answer to this question requires longitudinal research. Early behavioral models for the treatment of anxiety have been based on two primary suppositions. First, fears and phobias are acquired through classical conditioning, i. The neutral stimulus is then designated as a conditioned stimulus CS and the original aversive stimulus is called an unconditioned stimulus US. Second, the acquired fears can be unlearned through extinction, i. This conceptualization gave rise to exposure therapy, in which patients are taught to systematically confront their feared situations, objects, responses e.

While there have been debates about the mechanisms through which exposure therapy reduces anxiety symptoms, the benefit of this therapy has been demonstrated by a large body of research cf. Discontent with nonmediational automatic accounts for acquisition and extinction of pathological anxiety led to the development of theories that posited a pivotal role for cognitive factors in anxiety e. Meaning in these theories is often assumed to be represented in language. Accordingly, in cognitive therapy for anxiety disorders, verbal discourse is used to challenge the patient's threat interpretations of events and to help replace them with more realistic ones, especially so with adolescents.

With young children, however, cognitive therapy frequently takes the simpler form of thought replacement such that fearful thoughts are replaced with brave ones e. I can handle this. The focus on the meaning of events as accounting for pathological anxiety paralleled the reconceptualization of conditioning in learning theories. Obviously, for rats the meaning of events cannot be represented in verbal language; rather, it is represented as associations among stimuli, responses, and outcomes.

Advances in information processing theories of conditioning and of pathological anxiety e. One such conceptualization, emotional processing theory, was proposed by Foa and Kozak In this theory, fear is viewed as a cognitive structure in memory that serves as a blueprint for escaping or avoiding danger that contains information about the feared stimuli, fear responses, and the meaning of these stimuli and responses.

When a person is faced with a realistically threatening situation e. A fear structure becomes pathological when the associations among stimulus, response, and meaning representations do not accurately reflect reality; in this instance, harmless stimuli or responses assume threat meaning. In emotional processing theory, meaning is thought to be embedded in associations among stimuli, responses, and consequences as in Rescorla, , as well as in language, especially in the form of thoughts, beliefs, and evaluations as in Beck, Within emotional processing theory the anxiety disorders are thought to reflect the operation of specific pathological fear structures cf.

For example, the fear structure of individuals with panic disorder is characterized by erroneous interpretations of physiological responses associated with their panic symptoms e. As a result of this misinterpretation, individuals with panic disorder avoid locations where they anticipate experiencing panic attacks or similar bodily sensations, such as physical exertion. In contrast, the fear structure of individuals with OCD most p. Accordingly, the core pathology in panic disorder lies in the erroneous meaning of physiological responses, whereas the core pathology of OCD lies in the erroneous meaning of external events.

The supposition that inaccurate negative cognitions underlie the anxiety disorders has also been at the heart of theories posed by cognitive therapists e. If fear and avoidance reflect the activation of an underlying cognitive fear structure, then changes in the fear structure should result in corresponding changes in emotions and behavior. Indeed, Foa and Kozak proposed that psychological interventions known to reduce fear, such as exposure therapy, achieve their effects through modifying the fear structure.

According to emotional processing theory two conditions are necessary for therapeutic fear-reduction to occur: Thus, within this framework, exposure therapy is thought to correct the erroneous cognitions that underlie the specific disorder e. This is also the explicit mechanism by which cognitive therapy is thought to reduce fear. In this way the mechanisms that are thought to operate during exposure greatly overlap with those of cognitive therapy.

The cognitive approach to anxiety disorders comprises two research traditions McNally, b. In one tradition, researchers assume that introspective self-reports of anxious individuals can reveal aberrant cognition underlying symptom expression. These scholars administer questionnaires and conduct interviews to ascertain, for example, the intensity, frequency, and content of the worries and fears of children and adolescents.

Researchers in this tradition have also studied the fear of anxiety symptoms i. In the second tradition, researchers eschew self-report as insufficiently sensitive to measure abnormalities in cognitive mechanisms that often operate rapidly, and outside of awareness. Because attentional capacity is limited, people can attend only to certain stimuli at a given time, and any bias for selectively attending to threat-related stimuli should increase a person's likelihood of experiencing anxiety.

Most studies have shown that patients with anxiety disorders take longer to name the colors of words related to their threat-related concerns than to name the colors of other emotional or neutral words, and take longer to name the colors of threat words than do healthy subjects.

Although the emotional Stroop task has been traditionally interpreted as tapping an attentional bias for threat, debate continues about the mechanisms underlying the effect Williams et al. For example, the emotional Stroop may reflect an inhibitory problem rather than an attentional one. That is, delayed color-naming of trauma-related words may reflect difficulty suppressing the meaning of trauma-related concepts once they are activated rather than selective attention per se McNally, , pp.

Studies on the emotional Stroop in children have revealed mixed results. The magnitude of this trauma-related interference effect was unrelated to the age of the patients. However, not all Stroop studies have confirmed an anxiety-linked attentional bias for threat cues in youngsters. A second paradigm provides a much less controversial measure of attentional bias. On some trials, one word is threat related, whereas the other is not.

Coexisting Depression and Anxiety: Classification and Treatment

After the words disappear, a small dot replaces one of the words. Subjects press a button as soon as they detect the dot. Relative to healthy control subjects, patients with anxiety disorders are faster to respond when the dot replaces a threat word than when it replaces a neutral word. Because threat cues capture attention in anxious patients, these individuals are especially quick to respond to a neutral cue that follows a threat cue.

Using this task, Vasey, Daleiden, Williams, and Brown found that children ages 9—14 years with anxiety disorders exhibited an attentional bias for threat, whereas control children did not. The attentional bias increased with age and with reading ability. The GAD patients did not show an attentional bias for depression-related words, and the attentional bias for threat words was unrelated to the age of the subject.

Finally, patients with PTSD ages 9—17 years arising from either nondomestic violence or road traffic accidents ex p. Anxious children tend to interpret ambiguous information in a threatening fashion. In one study, children ages 7—9 years heard homophones e.

The higher a child's self-reported trait anxiety, the more likely the child selected threatening pictures e. In another study, GAD patients ages 8—17 years and healthy control children were shown homographs e. They were asked to construct a sentence including the homograph. Relative to the sentences constructed by control children, the anxious children more often constructed sentences incorporating the threatening interpretation of the homograph, implying that they had interpreted the ambiguous word in terms of its threatening meaning.

This interpretive bias was unrelated to the age of the subjects. Researchers asked anxious and nonanxious children to provide interpretations of ambiguous scenarios. Anxious fourth and fifth graders were more likely than their nonanxious peers to interpret nonhostile scenarios in a threatening fashion, whereas both groups interpreted ambiguous scenarios in a hostile fashion Bell-Dolan, This bias, however, was even more pronounced in patients with oppositional-defiant disorder.

Anxious children and adolescents exhibit threat-related attentional and interpretive biases that resemble those exhibited by anxious adults. Moreover, within most studies, the extent of bias did not vary as a function of the child's age. In one study, the responses of anxious children to two measures of attentional bias dot probe and emotional Stroop were uncorrelated, indicating that these tasks tap distinct constructs Dalgleish et al.

Further, researchers have yet to test whether these biases disappear following successful psychological or pharmacological treatment. A more detailed critique of information processing in adolescent psychopathology is available elsewhere Vasey et al. Although the exact timing of puberty is not easy to specify, scientists agree that the psychological and biological features of the era called adolescence are influenced by cultural setting.

Nonetheless, there is an identifiable period between 12 and 18 years, ubiquitous across societies, characterized by changes in hormones, brain structure, and behavior. The timing of pubertal signs is influenced p. The brain undergoes changes throughout life Eriksson et al. Periods of more dramatic change include not only pre-and early postnatal eras but also adolescence Spear, There is a similar loss of synapses in the human brain betwen 7 and 16 years of age Huttenlocher, , but the scarcity of human postmortem tissue makes it difficult to provide a more detailed description of this phenomenon.

Although the implications of the massive pruning remain speculative, it is likely that it reflects active restructuring of connections and the promotion of more mature patterns. The elimination of synapses that are presumed to be excitatory, accompanied by a reduction in brain energy utilization, transform the adolescent brain into one that is more efficient and less energy consuming Chugani, ; Rakic et al. Adolescence is also marked by changes in the relative volume and level of activity in different brain regions.

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For example, there is an increase in cortical white matter density reflected in myelinated fiber tracts and a corresponding decrease in gray matter, especially in frontal and prefrontal regions Giedd et al. The overall result of these varied changes is net decrease in the volume of the prefrontal cortex Sowell et al.

In the hippocampus and the amygdala however, gray matter volumes continue to increase during late childhood and adolescence Giedd et al. Lesions of the amygdala have opposite effects on fearfulness to social stimuli when those lesions are in infant versus adult monkeys Prather et al. Maturational changes in the cerebellum, and the circuitry connecting the cerebellum to the prefrontal cortex, continue through adolescence.

One consequence of this restructuring of the brain during adolescence is that early developmental compromises might be exposed. That is, brain regions vulnerable to dysfunction, due either to genetics or to adverse early experience, might be unmasked by the combination of brain restructuring and stressful life experiences Goldman-Rakic et al. There is great interest in detecting the biological variables that might distinguish anxious from nonanxious patients. There is debate over whether the amygdala is activated primarily by events that are potentially harmful or events that are unexpected or discrepant.

Support for the former, more popular, position comes from the elegant research of LeDoux , , and Davis , who have shown that acquisition of conditioned body immobility or bodily startle in rats, via Pavlovian conditioning with electric shock as the unconditioned stimulus, requires the integrity of the amygdala. But the amygdala also responds to discrepant and unexpected events that are harmless. Nonetheless, Ohman and Mineka argue that the amygdala reacts primarily to signs of danger rather than to novelty. They suggest that all animals inherit a fear module, located in the amgydala, that reacts without conscious awareness and free of cognitive control to events that pose a threat to the integrity of the body confrontation with snakes and spiders are classic examples of fear-evoking events.

There are serious problems with this theoretical position. First, the behavioral reactions of monkeys, chimpanzees, and human infants to a snake are no different from their reactions to discrepant events that are harmless for example, a tortoise or seaweed. The British psychiatrist Isaac Marks described the terror his 21 2 -year-old son displayed when he first saw thousands of dried skeins of seaweed.

However, the boy lost his fear following repeated exposures to these stimuli. If snakes were a biologically potent incentive for fear, a majority of monkeys should have shown an immediate withdrawal reaction.

Coexisting Depression and Anxiety: Classification and Treatment

It is relevant that discrepant events that pose no danger can produce the same level of amygdalar activation as dangerous ones. Adults in an fMRI scanner looking at faces with neutral expressions showed amygdalar activation to new, compared with familiar faces, even though no face had a fearful, disgusting, or threatening expression Schwartz et al.

Am J Psychiatry ; The definitive dictionary of psychiatry. Depression, anxiety and somatization in primary care: General Hospital Psychiatry ; Anxiety associated with comorbid depression. J Clin Psychiatry ; 63 suppl Effect of comorbid anxiety on treatment response and relapse risk in late-life depression: The association of depression and anxiety with medical symptom burden in patients with chronic medical illness.

Gen Hosp Psychyiatry ; Toward a unified treatment for emotional disorders. Behavior Therapy ; Depressive, anxiety, and somatoform disorders in primary care: Depress Anxiety ; 24 3: Frequency of anxiety disorders in psychiatric outpatients with major depressive disorder. Lydiard RB, Mintzer B. J Clin Psychiatry ; 59 suppl The pharmacologic treatment of mood disorders.

Psychiatr Clin North Am. Annual of Drug Therapy ; 1: Fava M, Rush J. Difference in treatment outcome in outpatients with anxious versus nonanxious depression: A Star D Report. Psychopharmacotherapy of panic disorder: Older patients with panic disorder and avoidance may have an increased risk of cardiovascular mortality.

The cause of panic disorder is unknown. Several factors probably contribute to its development, and no biological test is available. Genetic and early family factors, or both, are important. This leads to hypervigilance about bodily sensations, increased arousal of the sympathetic nervous system, more physical sensations, and heightened anxiety, which spirals into a panic attack.

Cognitive model of panic: A discrete period of intense fear or discomfort in which four or more of the following symptoms developed abruptly and reached a peak within 10 minutes:. Panic disorder can be caused by traumatic events, excessive caffeine, and misuse or withdrawal of drugs or alcohol. Evidence that hyperventilation causes panic attacks is conflicting. In the laboratory, prolonged hyperventilation can produce panic attacks. The diagnosis of panic disorder is relatively straightforward.

However, distinguishing panic attacks from medical disorders is difficult because symptoms that occur with panic attacks cover a wide range of medical problems. For example, about a quarter of patients who present with chest pain have panic disorder. In most of these patients, chest pain during the panic attack is not related to cardiac problems, but some may have panic attacks during times of myocardial ischaemia and the symptoms are similar. A careful history can usually lead to a diagnosis of panic disorder.

Diseases that can cause panic disorder, such as hyper-thyroidism, need to be ruled out. Panic disorder should be a positive diagnosis and not one of exclusion. Standard treatments are psychoeducation, psychotherapy particularly cognitive behaviour therapy , lifestyle changes, and drugs alone or combined. NICE guideline 22 concludes that psychotherapy, drugs, and self help bibliotherapy are effective and should be offered to patients, and patients' preferences and experience with previous treatment s should be taken into account.

Patients, families, and care givers should be informed of self help groups and support groups and encouraged to participate in such programmes if appropriate. Educating patients about the nature of panic disorder can be helpful and may be sufficient for patients without complications, although this assumption has not been tested in controlled studies.

The basic information can be presented in a handout, or patients can be referred to self help and internet resources. Patients should be encouraged to reduce caffeine intake, and sources of caffeine in the diet should be explained. Muscle relaxation techniques are useful and can be taught by using tapes or CDs, but relaxation proved less effective than behavioural and cognitive therapies in controlled trials. Exercise is often recommended to expose patients to increased heart rate and shortness of breath, but it has not been evaluated in controlled studies.

Stress management might be helpful, but it has not been systematically evaluated. Cognitive behaviour therapy comprises several cognitive and behavioural procedures. The rationale for this treatment derives from studies of fear habituation in animals. More recently, exposure therapy has been expanded to focus on real life situations or stimuli and the response to internal cues, such as high heart rate, hyperventilation, and dizziness.

A recent large, international, controlled study found that brief cognitive behaviour therapy six to eight hours of therapy, supplemented with hand held computers or manuals relieved panic attacks for most patients and was as effective as longer treatments. Retraining in breathing—where patients are taught to breathe slower, deeper, and more regularly—is a core feature of most psychological treatments for panic disorder, although its effectiveness is unconfirmed.

Cognitive behaviour therapy needs to deal with the cognitive aspects of panic and avoidance behaviour. Many patients who seem to be functioning well avoid activities that may hamper their performance, such as crossing bridges, making public presentations, or attending group meetings. Patients with panic disorder may develop elaborate ways of disguising their problems.

Antidepressants are the first line drug for patients with panic disorder: Few studies have shown differences between these inhibitors, and newer inhibitors are probably no more or less effective than older ones. Some patients experience restlessness, sweating, and tachycardia jitteriness syndrome when they start taking antidepressants.

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This might be avoided by starting at lower than usual doses. The effects of stopping these drugs may be especially upsetting to some patients with panic disorder, but the effects can be minimised by discontinuing the drugs over several weeks. Although these drugs are not associated with tolerance and craving, discontinuation or withdrawal symptoms may occur when the drug is stopped or doses are missed or, occasionally, when the dose is reduced.

These symptoms are usually mild and self limiting but occasionally can be severe, especially if the drug is stopped abruptly. Full guideline, section 12, pp Evidence for the effectiveness of other drugs is less compelling. Preliminary evidence shows that some of the newer antidepressants may also be effective. Benzodiazepines can be effective for treating panic disorder, but their use is controversial because of potential dependence, drowsiness, and impaired concentration. Benzodiazepines may interfere with the efficacy of cognitive behaviour therapy.

It may be difficult to withdraw patients from benzodiazepines, so they should be used sparingly.

What is panic disorder?

However, for patients with severe panic or in whom avoidance causes considerable work, family, or social problems, short term use of benzodiazepines may be indicated until psychological approaches and other drugs start to work. American Psychiatric Association http: National Institute of Mental Health www.

The Anxiety Association of America www. The National Phobics' Society www. Mastery of your anxiety and panic MAP Client workbook for anxiety and panic. Oxford University Press, —This book has been used successfully in evidenced based trials. The anxiety and phobia workbook. New Harbinger Press, —Avery popular book, but its effectiveness has not been evaluated in clinical trials. McGraw-Hill—Use of the book was effective as bibliotherapy in a randomised trial. A meta-analysis of the efficacy of psycho- and pharmacotherapy in panic disorder with and without agoraphobia. J Affect Disord ; Adding cognitive-behavioral therapy to pharmacotherapy for panic disorder:

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