Panic Lewis Psychiatry

8/12/2019 Panic Lewis Psychiatry

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Panic lewis psychiatry

Panic Disorder with or without Agoraphobia

Definition and Clinical Description

Panic disorder refers to the experience of unexpected panic attacks accompanied

by persistent apprehension about their recurrence or behavioral modifications in

daily routine as a result of the attacks. While panic attacks can occur in many

conditions, including phobias and social anxiety disorder, the panic attack

associated with panic disorder is unique in that it occurs spontaneously without an

environmental trigger. For example, panic disorder is uniquely associated with

nocturnal panic attacks, which spontaneously awaken a patient from sleep.

A panic attack is a discrete period of intense fear or discomfort that is

characterized by the presence of at least four somatic and/or cognitive symptoms.The most commonly reported symptoms among adolescents with panic attacks

appear to be trembling, dizziness/faintness, pounding heart, nausea, shortness of

breath, and sweating (43,44). Cognitive symptoms, such as a fear of going crazy

or dying, are reported less frequently than somatic ones (44). A diagnosis of panic

disorder with agoraphobia is indicated if the patient avoids places or situations in

which escape might be difficult or embarrassing. The most commonly avoided

settings include those involving large groups of people unknown to the patient,

such as restaurants, crowds, and auditoriums (43).

Specific Features

The most difficult distinction to make when diagnosing panic disorder in youth is

the difference between an unexpected panic attack, as required for a diagnosis of

panic disorder, and situationally cued attacks that are typical of other anxiety

disorders. This task becomes especially challenging given the cognitive

predisposition of children to attribute their experiences to external, identifiable,

situational factors. Careful attention to the circumstances surrounding attacks will

help with this distinction, as panic attacks occurring in the context of another

anxiety disorder will occur primarily in the presence of the target stimulus.

Additionally, presence of pervasive apprehension about having a panic attack, as

opposed to facing a feared stimulus, supports the diagnosis of panic disorder

rather than another anxiety disorder.Panic attacks can also be caused by a variety of medical conditions, including

hyperthyroidism, hyperparathyroidism, vestibular dysfunction, seizure disorders,

and cardiac abnormalities. Appropriate laboratory tests and physical examinations

should be used to rule out these causes prior to assigning a diagnosis of panic

disorder. In particular, when panic is accompanied by cardiac symptoms, a

discussion with a pediatrician as to the need for EKG and cardiac consultation is

encouraged.

Comorbidity

As in adults, anxiety disorders in youth are frequently comorbid with each other

and with other types of psychopathology. Rates of comorbidity among anxiety


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disorders tend to be somewhat lower in the general population 39% in children

(45,46) and 14% in adolescents (47) than in clinic samples (50%) (48). This

likely reflects a referral bias; children with multiple disorders, and consequentlygreater impairment, are more likely to seek treatment.

A recent community-based study found panic attacks and social phobia to be

highly comorbid with other anxiety disorders. Social anxiety was found to be

highly associated with any anxiety disorder (odds ratio [OR] = 14.2) (49). After

adjusting for differences in age and gender, the presence of panic attacks was

associated with increased likelihood of any anxiety disorder (OR = 4.6), social

anxiety (OR = 2.3), specific phobia (OR = 3.4), agoraphobia (OR = 2.9),

generalized anxiety disorder (OR = 4.8), overanxious disorder (OR = 3.7), and

separation anxiety disorder (OR = 3.1) (50). In clinic samples, SAD is found to be

more highly comorbid with other anxiety disorders than GAD and social phobia

(51). Children with SAD are more likely to have comorbid specific phobia thanchildren with GAD or social phobia. In contrast, children with GAD and social

phobia were more likely to have comorbid mood disorders as compared to

children with SAD. With respect to gender differences, in a nonreferred sample,

having more than one anxiety disorder during childhood and adolescence was

observed almost exclusively in females (52).

After comorbidity with another anxiety disorder, depression is the most

commonly reported comorbid condition among youth with anxiety disorders

(53,54). Depression is 8.2 times as likely in children with anxiety disorders than in

children without anxiety disorders (55). Specifically, there is a significant link

between GAD and depression that persists into adulthood (6). Children and

adolescents with GAD and comorbid MDD report significantly more anxiety

symptoms and demonstrate greater functional impairment than GAD youth

without MDD (56).

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Approximately 20% of children with an anxiety disorder also meet criteria for an

externalizing disorder (14,45,57,58). In a selective review of attention

deficit/hyperactivity disorder (ADHD), Biederman noted that about 30% of

children and adolescents with ADHD also have an anxiety disorder (59).

Interestingly, the prevalence of comorbid anxiety disorders increases in adultswith ADHD to approximately 50%. In both children and adults with ADHD,

females have a higher rate of comorbid anxiety disorders. Girls with the

inattentive subtype of ADHD have higher rates of comorbid SAD, while those

with the combined type have increased comorbidity with GAD (60). This is in

contrast to males with ADHD who have a higher prevalence of oppositional

defiant and conduct disorders.

Two additional conditions/disorders require mention when discussing comorbidity

of pediatric anxiety disorders. First, selective mutism, a disorder characterized by

persistent failure to speak in specific settings (school) despite full use of language

at home or with family, may be found in younger children with social phobia.

Approximately 68% of children with selective mutism also meet diagnostic


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criteria for social phobia (61). Second, while school refusal is not a DSM-IV

diagnosis, it is a condition that often cooccurs with anxiety disorders, specifically

SAD, specific phobia, and social phobia (62). School refusal is characterized bysignificant difficulty attending school, resulting in a prolonged absence and/or

severe emotional upset. These children often display excessive fearfulness, temper

outbursts, or complaints of feeling ill when faced with the prospect of going to

school (62). The nature of the anxiety associated with school refusal behavior is

likely to change with age, as is the nature of the precipitating events. For example,

fear of separation is more common in younger school refusers, while social-

evaluative fears, such as fears of teachers or peers, are more common in older

children.

Course of Pediatric Anxiety Disorders

Most prospective epidemiological studies examine the longitudinal outcome of

anxiety disorders, broadly conceptualized, as opposed to specific conditions(63,64). These studies find a statistically robust association between pediatric

anxiety and a range of adult conditions, including both mood and anxiety

disorders. However, from the standpoint of effect sizes, these associations are best

characterized as modest: Odds ratios tend to fall between 2.0 and 4.0, varying as a

function of severity and length of followup. This magnitude of association is

somewhat weaker than typically found in longitudinal studies of stability in

behavior disorders, such as conduct disorder. In terms of specific anxiety

disorders, relatively few longitudinal data examine outcome for any one

condition, compared with other conditions. Pine et al. (63) and Poulton et al. (65)

provide two of the few examples in community-based samples. While few

consistent associations emerge across these studies, data from both suggest that

GAD exhibits a robust association with a range of adult conditions, including

anxiety disorders and major depression. Data for other conditions, such as SAD or

social phobia, appear more variable. Some studies document specific outcomes in

these disorders (6), whereas other studies do not (65). Finally, similar conclusions

derive from longitudinal studies of pediatric anxiety disorders based in the clinic.

As with epidemiological studies, this research finds statistically robust

associations with medium effect sizes. While more evidence emerges in these

studies to support specificity of outcome, such as an association between SAD

and panic disorder, the evidence is far from compelling (22,24,25).

Etiological/Biological TheoriesAnxiety disorders, like most common psychiatric disorders, represent complex

conditions that result from interactions among multiple risk factors and underlying

predispositions. The majority of proposed etiological theories recognize the

complexity of causal pathways, leading to a general, comprehensive model. As

illustrated in Figure 5.5.1.1, this comprehensive model of anxiety disorders

focuses on four factors: 1) genetic and environmental influences, 2) neural

circuitry underlying emotion processing, 3) core psychological processes, and 4)

broad behavioral tendencies, including temperament. Each of these components

and their influences on the rest of the model will be discussed briefly in turn

(Figure 5.5.1.1).


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In terms of primary causes, this model implicates significant genetic and

environmental influences. Family and twin studies consistently note a strong

association between anxiety in parents and their children (29,66). Moreover, twinstudies among both children and adults document a statistically significant genetic

component to various forms of anxiety (66,67,68). These genetic and

environmental influences are unlikely to directly predispose toward anxiety

disorders per se. Rather, they are likely to shape more basic psychological

processes which in turn influence risk for anxiety. For example, there is evidence

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for genetic influences on fear conditioning, the process by which an association is

formed between a neutral stimulus, such as a tone or a light, and a noxious

stimulus, such as an electric shock (69). Elements of this process are believed to

underlie anxiety disorders, although the precise nature of the relationship betweenfear conditioning and anxiety remains ill specified (70).

FIGURE 5.5.1.1. Etiological model of pediatric anxiety disorders.

In terms of specific genetic contributions, recent studies have focused on a

polymorphism in the promoter region of the serotonin transporter gene (5HTT)

involving a 44-bp insertion or deletion. As noted above, in the discussion of GAD,

individuals with the short form of the gene (ss or sl) have been shown to have

higher neuroticism, harm avoidance, and anxiety than individuals homozygous for

the long variant (ll) (71,72). A polymorphism of the variable-number-tandem-

repeat in the second intron of the serotonin transporter gene has also been

associated with increased risk of anxiety disorders, including OCD and GAD (73).

Despite such evidence of a genetic contribution, anxiety disorders generally

involve a large environmental component. From an environmental perspective,

parents with anxiety disorders may use distinctive child rearing practices that

affect risk for anxiety (66,74). For example, parents of anxious youth have been

shown indirectly and directly to encourage maladaptive patterns of responding to

ambiguous situations (75), exhibit overcontrolling and intrusive behaviors

(76,77,78), and model anxious behavior themselves (79). As such, familial

associations between parent and child anxiety may result through direct effects of

these parenting behaviors, or through interactions between parentchild

relationships and a genetically predetermined diathesis. Similar to genetic effects,

these influences are unlikely to directly predispose towards anxiety. Rather, theyare likely to shape core psychological processes, which in turn give rise to anxiety

disorders.

There is increasing interest in understanding the interaction between genetic and

environmental factors in the development of anxiety disorders. One recent report

found an interaction between maternal reports of social support and child 5-HTT

status in predicting behavioral inhibition at age 8 (80). Further research on similar

interactions will allow for more comprehensive pathophysiologic models of

anxiety disorders.

As noted above, the primary causes of anxiety, as reflected in genetic and

environmental risk factors, influence the development of anxiety by shaping core

psychological processes, such as fear conditioning. These psychological processes


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reflect the influence of genes and the environment on functional aspects of brain

regions involved in fear and reward circuits. These regions include structures of

the striatum as well as limbic and paralimbic systems, including the amygdala,orbitofrontal cortex (OFC), and anterior cingulate cortex (ACC)

(81,82,83,84,85,86). These areas are highly interconnected and play a significant

role in the integration of internal and external experience of emotion.

Animal and human studies provide indisputable evidence that the amygdala plays

an important role in fear conditioning, a basic process by which fear toward a

previously neutral stimulus develops. As a result, it has been implicated as a

critical element of the neural circuitry underlying anxiety disorders (87). This is

supported by neuroimaging findings that show that anxiety-disordered adults and

children demonstrate greater amygdala activity in response to face stimuli than

controls (88,89,90). In children, the magnitude of the signal change between

fearful and neutral faces has been shown to be positively correlated with childself-report ratings of anxiety (90). A recent study found that this anxiety-related

amygdala response to fearful faces is greater when the child attends to his/her

internal emotional state than to the features of the face itself (91).

Structural imaging studies also document abnormalities in the amygdala among

children and adolescents with anxiety disorders. For example, recent voxel-based

morphometry findings show decreased left amygdala volume in children with

anxiety disorders (92). These results, together with the functional neuroimaging

findings, suggest an excitotoxic process may occur in the anxiety disorders,

through which amygdala volume is reduced and responsivity increased. This

theory of excitotoxicity as a risk factor for psychopathology was first introduced

as a model for MDD (93). In light of the association between childhood anxiety

disorders and MDD, it is a plausible model for these disorders as well.

Nevertheless, relatively few studies examine amygdala volume in the anxiety

disorders, and findings appear inconsistent: At least one group has reported an

increased amygdala volume in pediatric GAD (94).

Beyond the amygdala, the orbitofrontal cortex (OFC) represents a second

structure directly implicated in aspects of emotion processing that are perturbed in

anxiety disorders. This includes the flexible representation of both negative and

positive reinforcers (95). As such, it is likely a critical element of the neural

circuitry of anxiety and anxiety disorders. In support of this theory, anxiety

induction studies have demonstrated increased activation in areas of the rightprefrontal cortex (96,97) and left OFC (98). Pooling data across three groups of

anxiety-disordered adults, Rauch and colleagues found consistent activation of the

right medial OFC during symptom provocation (99). Magnetic resonance

spectroscopy (MRS) studies demonstrate anxiety-related alterations in chemical

composition of the OFC that are suggestive of changes in neuronal viability

(100,101). Monk et al. (102) report comparable perturbations in pediatric anxiety

disorders.

Through its connections to the OFC and amygdala, the anterior cingulate cortex

(ACC), particularly the rostral-ventral portion, serves to regulate emotional

responses, and therefore is likely to be involved in the neural circuitry of anxiety.

Studies of healthy adults using anxiety induction have demonstrated a decrease in


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activity in ACC (103,104). A similar result has been found in patients with

posttraumatic stress disorder (PTSD) who fail to demonstrate normal activation of

the rostral ACC when shown combat-related stimuli (105). Through connectionswith the PFC, this dampening of the rostral ACC signal might serve to lessen

cognitive control over threat-related information, which likely leads to the distress

characteristic of patients with PTSD when exposed to trauma-related stimuli. In

contrast, Rauch et al. (106) used PET to examine regional cerebral blood flow

changes in patients with specific phobias during symptom provocation and found

significant increases in the ACC, as compared to a control condition. These

conflicting results suggest that specific phobias may rely on a different neural

mechanism than other anxiety disorders.

According to this general model, perturbations in this core circuitry contribute to

anxiety disorders through their effects on anxiety-related biases in information-

processing functions. These functions can be conceptualized as core psychologicalprocesses, such as attention and motivation. Independent of research on brain

imaging or neural circuitry function, a wealth of research examines the association

between variations in anxiety and various core psychological processes. In

experimental work, the most consistent cognitive feature associated with fear and

anxiety in humans represents an attention bias for stimuli associated with danger

(107,108,109,110,111). This bias resembles the high degree of vigilance that

animals show for feared scenarios or objects. In human studies, it is most often

measured using the dot probe and Stroop paradigms.

In the dot probe task, individuals monitor two stimuli presented on a computer

screen: One is either a threatening word or picture and the other is a neutral word

or picture.

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Subjects must press a button when a target appears in place of one of the stimuli,

and reaction times to these targets are influenced in individuals with high levels of

anxiety by proximity between the threat cue and the target. Studies using dot

probe tasks demonstrate a bias toward threatening stimuli in adults and children

with anxiety disorders that is not seen in nonanxious controls

(112,113,114,115,116). Recording of eye movements during a face dot probe task

confirmed that patients are more likely than normal controls to initially look

toward a threatening face than a neutral one (117). Interestingly, this orientingtoward threat is more likely to occur with brief stimulus presentations (500 ms),

suggesting cognitive mechanisms early in information processing (116).

The Stroop task requires subjects to name the color of potentially threatening

words, such as coronary or snake. Prolonged latency for naming

such color-words is presumed to be the result of interference, such that reactions

elicited by a fear word interfere with attention to the color of the word. This effect

has been demonstrated in both adults (118,119,120,121) and children (122) with

anxiety disorders. While similar degrees of attention bias are found across anxiety

disorders, the particular stimuli that cause this bias differ. For example, panic

disorder patients may show a particularly prolonged latency to panic-related


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words, such as smother, while subjects with social phobia may show

greater latencies to relevant words such as embarrass.

This bias toward threat is also evident in interpretations of ambiguity. Childrenwith anxiety disorders have been shown to be more likely to interpret ambiguous

stimuli as threatening. When performing a homophone task during which the

subject is asked to write down words he hears on an audiotape, GAD patients

display a greater tendency to write down the word associated with the more

negative interpretation (pain vs. pane) (123). In a homograph study where children

were shown a list of words with neutral and threatening meanings, youth with

GAD showed a greater tendency to produce sentences using threatening

interpretations than control participants (124). Similar results are found in studies

when children diagnosed with anxiety disorders are presented with ambiguous

situations and asked to interpret them (75,125). Anxiety-disordered youth are

more likely to make a threatening interpretation of these situations than theirnonanxious peers.

Finally, these core psychological processes are believed to underlie broad

behavioral tendencies such as early temperament and later development of anxiety

disorders. Behavioral inhibition is a temperamental factor measurable during the

first years of life that has been shown to predict later onset of anxiety disorders

(126,127). Children with temperaments characterized by behavioral inhibition

react to novel situations with signs of reticence or withdrawal. Based on

peripheral physiologic data, behavioral inhibition is thought to result from an

underlying hypersensitivity within amygdala-based neural circuits (126). While

most children with behavioral inhibition do not develop clinical anxiety disorders,

behavioral inhibition does predict an elevated risk for childhood anxiety disorders,

particularly social phobia (32).

Clearly, the development of anxiety and its disorders is a complex process that

likely involves biological vulnerabilities as well as environmental influences.

Significant advances in basic research have provided a neurobiological framework

on which to base hypothesized etiological models. Additionally, advanced

research technologies in genetics and neuroimaging have allowed us to test these

models with ever increasing sophistication and detail. Continued translation of

basic research findings to clinical studies will be essential to the further

advancement of our understanding of anxiety disorders.

Treatment of Pediatric Anxiety DisordersOver the past two decades, significant advances have been made in the treatment

of pediatric anxiety disorders. Cognitive-behavioral and pharmacological

interventions have emerged as effective treatments for these disorders. While a

few trials have evaluated these treatments for a specific anxiety disorder, most

have included children and adolescents with a primary diagnosis of GAD, SAD,

or social phobia. In light of the high comorbidity among these disorders, this

approach improves the feasibility and generalizability of these studies. The most

widely used interventions and their empirical support will be discussed here.

Cognitive-Behavioral Interventions

Cognitive-behavioral treatments (CBT) have proven to be effective at treating

anxiety disorders in children and adolescents (128,129,130). Most cognitive-


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behavioral interventions were initially developed for adult anxiety and phobic

disorders, so the techniques for children are conceptually and structurally similar

but modified according to developmental level. For example, to introducecognitive restructuring, these treatments use cartoons and thought bubbles to help

children learn to identify and then change their thoughts. In addition to cognitive

techniques, these treatments include behavioral strategies such as modeling,

relaxation skills training, homework, contingency management, and most

importantly, exposure to feared situations. The aim of exposures, either imaginal

or in vivo (real life), is to provide the patient with opportunities to practice newly

learned coping skills in a safe, controlled environment. Feared stimuli or

situations are presented in a graduated fashion, beginning with the easiest and

ending with the most difficult, so that the child experiences early success in using

these new skills. The pace at which the child and therapist move up the hierarchy

is determined by these successes.Empirical evidence supports the use of these cognitive-behavioral interventions

for pediatric anxiety disorders. Kendall et al. conducted two randomized-

controlled trials demonstrating the efficacy of a 16-week individual CBT for

children with social phobia, GAD, and SAD (129,130). Treatment gains were

maintained at 1, 3 (131), and 7 years post-treatment (132). Barrett and colleagues

modified Kendall's CBT and added a family-based component that teaches parents

how to be effective models for their children and how to encourage coping with

feared situations, rather than avoidance. Individual CBT plus the family

component was shown effectively to reduce anxiety symptoms and may have had

some added benefits, particularly for younger, female children (128). Treatment

gains were maintained at 6-year follow-up (133). Group cognitive-behavioral

interventions have been shown to be effective for the treatment of socially phobic

children and adolescents (134,135,136). Conducting treatment in a group setting

provides these children with greater opportunities for in vivo exposures.

While this work clearly documents the benefits of CBT in pediatric anxiety

disorders, major questions remain concerning the mechanism of these effects.

Such questions emerge given limitations in the available studies. In particular, the

majority of controlled trials compare CBT to relatively crude comparison

conditions, such as a wait-list control. A few trials have used more rigorous

designs, whereby a credible attention-control condition is used. Results in these

trials are less consistent than in the trials comparing CBT to a wait-list (137,138).Nevertheless, at least one study in pediatric social anxiety disorder demonstrated a

superior response to

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CBT relative to a credible attention-control intervention. Moreover, ongoing

studies are comparing CBT for pediatric anxiety disorders to placebo control.

Findings in pediatric MDD using this same contrast recently generated

considerable questions on efficacy of CBT in this condition. Results from the

comparison of CBT with placebo in the anxiety disorders are thus eagerly

anticipated. A more detailed discussion of CBT appears in Chapter 6.2.2.

Pharmacological Interventions


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Advances in psychopharmacology and the design and implementation of large

placebo-controlled studies have led to significant improvement in the treatment of

pediatric anxiety disorders. As with CBT, pharmacological agents that have beenshown effectively to treat adult anxiety disorders, such as antidepressants and

anxiolytics, are now being used to treat children. Benzodiazepines have shown

mixed results (31,139) and are not indicated as a first-line treatment in children

due to their potential adverse effects. There is also little or no evidence for the

efficacy of other anxiolytics, such as buspirone or beta-blockers. While tricyclic

antidepressants have demonstrated some efficacy, they have not been shown

convincingly to treat pediatric anxiety disorders, beyond the data documenting the

efficacy of clomipramine for pediatric OCD. In addition, their side effect profiles

do not make them a viable first-line treatment option for children. Overall,

efficacy and safety data support the use of selective serotonin reuptake inhibitors

(SSRIs) to treat childhood social phobia, SAD, and GAD. In light of this, thissection will review only current findings regarding the treatment of pediatric

anxiety disorders using SSRIs. A greater discussion of psychopharmacologic

agents appears in Chapter 6.1.

Early open trials of SSRIs showed promising results for children with mixed

anxiety disorders (140,141). Following from these results, the Research Unit on

Pediatric Psychopharmacology (RUPP) conducted the largest medication trial of

children (ages 617) with a primary diagnosis of SAD, GAD, or social phobia

(142). Following a 3-week supportive psychoeducational treatment lead-in, 128

children were assigned to either fluvoxamine or placebo for 8 weeks. The children

in the fluvoxamine group had greater reductions in symptoms of anxiety and

higher rates of clinical response than the children in the placebo group. On the

Clinical Global Impression scale, 48 of 63 (76%) children in the fluvoxamine

group were classified as treatment responders, in comparison to only 19 of 65

(29%) children in the placebo group (p < 0.001). In a somewhat smaller

randomized placebo-controlled study of 74 children with GAD, social phobia,

and/or SAD, fluoxetine was found to be superior to placebo in decreasing

symptoms of anxiety (143).

Recent studies have demonstrated the efficacy of SSRIs for specific anxiety

disorders. For example, Rynn et al. conducted a placebo-controlled study of

sertraline with children and adolescents with GAD (144). Beginning at 4 weeks,

the sertraline-treated group showed significantly reduced scores on the Hamiltonanxiety scale and the Clinical Global Impression (CGI) severity and improvement

scales. Recently a multicenter, randomized, double-blind, placebo-controlled trial

of children and adolescents with social anxiety disorder concluded that paroxetine

is an effective, generally well tolerated treatment for social phobia (145). A total

of 322 children and adolescents age 817 either received placebo or paroxetine

(1050 mg/day) for 16 weeks. As measured by the CGI-Improvement scale, the

odds of responding were significantly greater for paroxetine versus placebo.

There have been no placebo-controlled, double-blind trials of the treatment of

panic disorder in children. A small, open label study of 12 children and

adolescents with panic disorder showed improvement on SSRIs with minimal side

effects (146). In a preliminary naturalistic study, 15 of 18 children and adolescents


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with panic disorder were considered responders to paroxetine (147). In adults,

SSRIs have become the pharmacotherapeutic treatment of choice, and several

SSRIs have approved indications for the treatment of panic.Questions have been raised about the safety of SSRIs in children and adolescents.

In particular, the Food and Drug Administration (FDA) issued a black

box warning in the fall of 2004 concerning the use of SSRIs in this age group.

This warning cautioned physicians about the possible adverse behavioral side

effects of SSRIs. Specifically, analyses performed by the FDA demonstrated a

higher rate of suicidal thoughts and acts in a metaanalysis of randomized

controlled trials. These trials had examined approximately 4,000 children and

adolescents with various forms of psychopathology, including anxiety. While the

overall rate of clinically significant suicidal thoughts or acts was less than 5%, the

rate was statistically greater for individuals randomized to SSRIs as compared to

placebo. As a result, prescribing clinicians need to be very careful to assess forsigns of behavioral activation and/or suicidality when using these treatments. It is

also especially important to take a careful history before prescribing that includes

signs of mood instability in the patient or family members.

Future Directions/Research Challenges

Over the past 20 years, significant strides have been made in the development of

effective treatments of pediatric anxiety disorders. Cognitive-behavioral

treatments and SSRIs have proven to be first-line interventions. However, we

have little information about which is more effective, and for whom. The next step

is to conduct a study examining these issues. Are medications more effective than

CBT; is CBT more effective than medication? Is the combination of CBT plus

medications more effective than either alone? Such a study is currently underway

and we will have to await the results.

In conclusion, this chapter has provided a review of pediatric anxiety disorders,

including current findings regarding their prevalence, etiology, and treatment. The

study of these disorders is relatively new, as compared to other psychiatric

conditions (schizophrenia, major depressive disorder). As a result, our

understanding of underlying developmental and neurobiological mechanisms is

limited. Continued advances in basic science research, genetics, and neuroscience

will allow for further refinement of current models and subsequent development

of new interventions for the prevention and treatment of pediatric anxiety

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