Anxiety disorders are the most prevalent mental disorders, with a global current prevalence estimate of 7.3%1. An early construct was “anxiety neurosis”, but this was poorly operationalized. The differentiation of specific anxiety disorders in the DSM-III was therefore an important step forward for the field, giving impetus to the development of a more personalized approach to the treatment of the individual patient with anxiety2. An early hypothesis, for example, was that patients with social anxiety disorder would respond preferentially to monoamine oxidase inhibitors3.

At the same time, anxiety disorders are characterized by significant comorbidity, and each disorder is heterogeneous in terms of phenomenology and psychobiology. Thus, for example, social anxiety disorder is often accompanied by generalized anxiety disorder (GAD), and ranges from discrete social anxiety disorder to generalized social anxiety disorder4. Although there is a large body of evidence on the value of selective serotonin reuptake inhibitors (SSRIs) and cognitive-behavioral therapy (CBT) for anxiety disorders, this heterogeneity may explain why a significant proportion of individuals do not respond to first line therapy5.

While current diagnostic systems are certainly useful in formulating an initial treatment plan, it behooves the field to develop additional decision support tools. These may allow us to move away from guidelines that focus solely on disorders and that emphasize SSRIs and CBT as first line steps towards more detailed assessments that provide the clinician with more specific guidance and facilitate a more personalized approach. More detailed and rigorous matching of presentation with management may ultimately improve treatment outcomes6.

This paper aims to describe systematically important domains relevant to the personalization of management of anxiety disorders and related conditions such as obsessive-compulsive disorder (OCD) and post-traumatic stress disorder (PTSD) (Table 1). For each domain, we summarize the available research evidence and review the relevant assessment instruments, paying special attention to their suitability for use in routine clinical practice. We emphasize areas where the available evidence allows the clinician to personalize the management of anxiety and related conditions, and we point out key unmet needs. The research literatures on anxiety and depression have many important overlaps, so it is not surprising that this list of domains draws closely on previous work on depression6.

Table 1. Salient domains to be considered in the clinical characterization of a patient with an anxiety or related condition 1.Symptom profile Clinical subtypes Severity Neurocognition Functioning and quality of life Personality traits Antecedent and concomitant psychiatric conditions Physical comorbidities Family history Early environmental exposures Recent environmental exposures Protective factors / Resilience Dysfunctional cognitive schemas

In keeping with the aims of precision medicine, considerable effort has been paid to developing biomarkers for anxiety and related disorders. It is notable that fear conditioning and extinction provide an important paradigm for explaining the symptoms of these disorders, as well as conceptualizing treatment approaches7. Additional specific constructs, such as cognitive flexibility and inhibitory control, may be more relevant to particular disorders, such as OCD8. These concepts are emphasized in the translational neuroscience framework of the US National Institute­ of Mental Health’s Research Domain Criteria (RDoC)9 and contributed in part to the separation of anxiety disorders in the DSM-5 and ICD-11 into anxiety or fear-related disorders, obsessive-compulsive and related disorders, and disorders specifically associated with stress (these are the terms used in the ICD-11)10.

Despite the extent and rigor of research on the neurobiology of anxiety and related disorders, no biomarker of these conditions has to date proven sufficiently sensitive and specific for widespread adoption in clinical practice11, 12. We therefore do not address biomarkers in detail in the current paper. However, we hypothesize that more personalized assessment of the sort proposed herein may be useful in advancing biomarker research, as well as work on the translational neuroscience of anxiety more generally, given the potential value of more fine-grained clinical assessments for delineating disorder heterogeneity in ways that may be neurobiologically informative and which may predict treatment response6, 13.

The paper focuses on anxiety and related disorders in the adult patient. These disorders often have an early onset, and pediatric anxiety is important both clinically and from a public health perspective; additional work is therefore needed to address the child and adolescent with anxiety. We also do not address in detail anxiety secondary to other mental disorders such as major depression or a psychotic disorder, or anxiety due to another medical condition, or anxiety induced by a substance or a medication, despite their clinical significance. Nor do we closely cover issues relevant to subthreshold anxiety and related disorders, despite their public health importance14. Gender- and culture-related issues are considered where relevant.

SYMPTOM PROFILE

Anxiety disorders share features of anxiety, fear and/or panic attacks, often accompanied by phobic avoidance or overly cautious behaviors, in reaction to perceived threats. In both the DSM-5 and ICD-11, anxiety disorders include agoraphobia, GAD, panic disorder, selective mutism, separation anxiety disorder, specific phobia, and social anxiety disorder. OCD and PTSD are included in separate but closely related groupings. In both nosologies, the diagnosis of anxiety disorders involves marked or substantial levels of fear or anxiety, that differ from stress-induced transient fear or anxiety by being persistent (i.e., lasting several months or more) and distressing or impairing.

Both the DSM-5 and ICD-11 differentiate among the anxiety disorders primarily by the focus of apprehension (i.e., perceived threat) and the types of objects or situations that induce anxiety, fear or panic attacks. The perceived threat and associated stimuli range from being tightly circumscribed (as in specific phobia), to domain-specific (as in agoraphobia, panic disorder, separation anxiety disorder, and social anxiety disorder), to pervasive (as in GAD). Thus, although highly comorbid with one another, anxiety and related disorders can be differentiated by close examination of the range and types of situations that are feared or avoided and the content of the associated thoughts or beliefs. For example, panic disorder is characterized by fears of interoceptive cues which are misappraised as being harmful, whereas social anxiety is characterized by fears of social or performance situations in which negative evaluation and rejection is anticipated to occur. Differentiation between the anxiety and related disorders is of high relevance to clinical management and treatment selection, since most evidence-based pharmacological and psychological treatments are tested for specific anxiety or related disorders.

The most significant difference between the DSM-5 and ICD-11 conceptualizations of anxiety and related disorders is in the diagnostic requirements for PTSD15. In the DSM-5, the criteria were expanded substantially, to include twenty symptoms across four clusters, in an attempt to capture the full scope of chronic post-traumatic expressions. In contrast, the ICD-11 simplified PTSD diagnostic requirements to three core symptoms that most clearly distinguish this disorder from other conditions, i.e. re-experiencing the traumatic event or events in the present, deliberate avoidance of reminders, and a sense of ongoing threat. Evidence suggests that the data better fit the simpler factor structure of the ICD-11 than the DSM-5 criteria16. The ICD-11 defines “complex PTSD” as consisting of the three core PTSD symptoms described above accompanied by problems in affect regulation, negative self-beliefs, and relationship difficulties17. Latent class analysis and latent profile analysis have supported the distinction between PSTD and complex PTSD as well as the association between complex PTSD and trauma in childhood in some studies16.

Anxiety disorders are marked by fear or anxiety. Fear is conceptualized as the emotional response to perceived predictable or imminent threat when there is little or no time to consciously strategize escape, whereas anxiety is a future-oriented state of anticipation for uncertain, prolonged or distal threats when there is time to comprehend the foreboding nature of the situation. Both states are designed to activate cognitive, affective, physiological and behavioral processes that enhance safety. In the case of fear, rapid, involuntary, physiological reactions facilitate the selection and production of an appropriate fight or flight response; whereas anxiety activates physiological and cognitive strategic preparation for fight or flight if needed18-20. This view of fear and anxiety is supported by animal predatory imminence continuum models that posit distinct modes (from pre-encounter potential for threat, to post-encounter threat detection, to circa-strike predator attack) that each result in distinct well-defined behaviors and defensive circuits21.

These canonical modes of threat are universal (although the responses are species-specific) and applicable not only to non-primates but also to humans22, 23. Optogenetic studies in non-primates show that stimuli analogous to pre- and post-encounter threats evoke the ventromedial prefrontal cortex, hippocampus, and basolateral amygdala – regions involved in threat memory, prospection and avoidance24, 25. In the circa-strike attack mode, activity is evoked in circuits that include the mid-cingulate cortex, central amygdala, hypothalamus, and periaqueductal gray – regions involved in fast reactions to threat (e.g., flight)24, 25. Similar defensive circuits exist in humans: functional magnetic resonance imaging (MRI) studies show that distant threat is associated with increased activity in the ventromedial prefrontal cortex, and, as threat moves closer, more activation in midbrain periaqueductal gray is observed26, 27. The RDoC, which take a dimensional approach to psychopathology, draw upon these models by suggesting that “responses to low imminence threats are qualitatively different than the high imminence threat behaviors that characterize fear”9.

Whereas prototypes of fear and anxiety lie at different “places” upon a continuum of responding, clinical presentations are more fluid. For example, perceptions of threat can rapidly change from being distal to imminent through appraisals and imagery alone, without change in external circumstances. An exemplar is the person with PTSD who experiences a fearful flashback to trauma (i.e., imminent threat) in the midst of anxiety in unfamiliar surroundings (i.e., distal threat).

Anxiety and fear are expressed across multiple response modalities: behavior, physiology and subjective report28. States of anxiety are typically linked with behaviors of vigilance, caution and avoidance, physiological preparation for acute threat (e.g., startle response amplification, elevated muscle tension), statements of worry or concern, and appraisals of impending or uncertain threat (e.g., “What if I mispronounce a word at the dinner party next week – I will be so embarrassed” or “What if I faint in the movie theater”). States of fear are linked with behaviors of escape (or fight), autonomic arousal, statements of fear or fright, and appraisals of acute threats (e.g., “I am dying” or “I need to get out of here”)29.

Notably, these response modalities are not always concordant30. For example, individuals may report anxiety or fear in the absence of physiological changes or behavioral outputs, or may avoid situations in the absence of reported anxiety or fear. Even during panic attacks, people sometimes report fear without evidence of physiological changes31. Such discordance may be informative for treatment selection. For example, subjective distress in the absence of physiological changes may indicate the value of a cognitively oriented treatment approach rather than a biologically oriented one (such as respiratory regulation or pharmacotherapy), and behavioral avoidance in the absence of physiological changes may indicate the particular value of exposure therapy. However, evidence for such treatment matching remains only nascent, as clinical trials have focused primarily on particular anxiety diagnoses and clinical subtypes, rather than on detailed assessment of specific behaviors, physiological parameters, or cognitive appraisals.

In clinical practice, the key first step in the assessment of anxiety symptoms is the establishment of an anxiety or related disorder diagnosis on the basis of the symptom profile. The diagnosis of anxiety and related disorders in adults can be ascertained using validated clinical interviews. Examples of such interviews include the Structured Clinical Interview for DSM-5 (SCID-5)32, the Mini International Neuropsychiatric Interview (MINI)33 and the Composite International Diagnostic Interview (CIDI)34. The Anxiety and Related Disorders Interview Schedule for DSM-5 (ADIS-5) is particularly focused on the differential diagnosis among anxiety disorders35. A structured diagnostic interview for obsessive-compulsive and related disorders may be useful for assessing this range of often overlooked conditions36.

Determining whether the anxiety symptoms (for example, panic attacks) are occurring as a manifestation of another mental disorder (such as major depression or bipolar disorder) is important. Substance use or intoxication (e.g., use of caffeine, stimulants) and withdrawal (e.g., from alcohol use) can lead to prominent anxiety symptoms. Certain medical conditions also produce anxiety symptoms, such as cardiopulmonary (e.g., asthma), endocrine (e.g., thyroid disease) and neurological (e.g., complex partial seizures) disorders, among others.

Identifying anxiety related to medical conditions is achieved through a detailed medical history and physical examination and, when warranted, specific blood (e.g., thyroid-stimulating hormone levels) or other (e.g., electrocardiography or electroencephalography) tests. Although structural (for example, voxel-based morphometric) and functional MRI have been used to learn more about the pathophysiology of anxiety and related disorders, they are not currently useful for diagnostic purposes11, 12.

Data on the underdiagnosis and undertreatment of anxiety and related disorders underscore the importance of screening for anxiety symptoms37. The Generalized Anxiety Disorder-7 (GAD-7)38 is a 7-item self-report questionnaire that has been developed specifically for GAD, but has been found to be useful in identifying any anxiety disorder with adequate sensitivity and specificity39. Other screening tools include the Hospital Anxiety and Depression Scale40 and the Overall Anxiety Severity and Impairment Scale (OASIS)41, which includes measurement of avoidance behavior (an important feature, since anxiety levels may be masked without such measurement). The Perinatal Anxiety Screening Scale is suitable as a nonspecific screener for perinatal women42.

If an anxiety or related disorder is present, several measures can be used to assess the profile of anxiety symptoms. The Interview for Mood and Anxiety Symptoms assesses all symptoms of DSM and ICD emotional disorders as well as other manifestations of internalizing psychopathology43. Each item is rated from clearly absent, to partially present (subclinical, subthreshold) to clearly present, and thus symptom profile scores can be evaluated. Aside from interviews, self-report questionnaires exist for each of the anxiety and related disorders, and provide more detailed symptom profiles. These include the DSM-5 scales developed for agoraphobia, GAD, OCD, PTSD, social anxiety disorder, and specific phobia, each one including items for affective states of fear and anxiety, physiological, cognitive and behavioral symptoms44. With the exception of specific phobia, these scales have been shown to have adequate to strong psychometric properties45-52.

A number of other well-validated standardized symptom questionnaires exist. They include the Penn State Worry Questionnaire53 for GAD; the Yale-Brown Obsessive-Compulsive Scale (Y-BOCS)54 for OCD; the Albany Panic and Phobia Questionnaire-Agoraphobia55, the Mobility Inventory for Agoraphobia56, the Panic Disorder Severity Scale57, and the Panic and Agoraphobia Scale58 for panic disorder and agoraphobia; the PTSD Checklist-5 for DSM-5 (PCL-5)59 and the Clinician Administered PTSD Scale for the DSM-5 (CAPS-5)60 for PTSD; and the Social Phobia and Anxiety Inventory61 and the Liebowitz Social Anxiety Scale62 for social phobia. Scales for each type of specific phobia are not available, but a generic measure is the Fear Survey Schedule63, a 51-item questionnaire that asks respondents to indicate their discomfort, or felt anxiety, to each of fifty-one stimuli.

Distinguishing the anxiety and related disorders can guide clinicians to disorder-based treatment. Particular versions of CBT have been developed to target the specific focus of apprehension of each anxiety or related disorder. There is a substantial evidence for the efficacy of such targeted treatments64-66, and they are recommended as first-line psychological treatments for anxiety and related disorders in several guidelines, including those by the UK National Institute for Health and Care Excellence (NICE)67. For example, CBT for panic disorder includes interoceptive exposure to feared bodily sensations; CBT for social anxiety disorder includes cognitive restructuring around post-event rumination; CBT for GAD addresses meta-beliefs about worry; CBT for OCD includes exposure to specific cues that trigger distress and the urge to perform compulsive rituals as well as response prevention aimed at eliminating the compulsions; and CBT for PTSD includes imaginal exposure or cognitive reprocessing regarding trauma memories. Thus, differential diagnosis facilitates choice of the most appropriate form of CBT. Even if using transdiagnostic CBT, a promising alternative to disorder-specific approaches68, the clinician will still need to implement the therapeutic strategies in ways that are tailored to each person’s focus of apprehension.

In terms of pharmacotherapy, SSRIs have demonstrated efficacy for all major anxiety and related disorders. Nevertheless, it is important to distinguish between the various disorders, for several reasons. First, SSRI pharmacotherapy guidelines differ across the various anxiety and related conditions69. Thus, for example, it is particularly important to begin with lower doses of an SSRI in panic disorder (as standard doses may not be tolerated), while a higher dose and longer duration of treatment is particularly important in OCD. Second, agents other than SSRIs have different efficacy across different anxiety and related disorders69. Thus, for example, the tricyclic antidepressant imipramine is efficacious in some anxiety and related disorders (e.g., GAD, panic disorder, PTSD) but not others (OCD, social anxiety disorder); the benzodiazepine alprazolam is efficacious in a different range of anxiety disorders (GAD, panic disorder, social anxiety disorder) but not in anxiety related disorders (OCD and PTSD); buspirone is efficacious in GAD but not in other anxiety and related disorders, while OCD appears unique among these conditions in being more responsive to serotonergic than noradrenergic re­uptake inhibitors69.

Greater precision and ultimate efficacy may derive from matching treatment to symptom clusters, given the heterogeneity that exists within diagnostic labels. Indeed, there is evidence that clinicians already view symptom clusters as more informative than diagnostic categories for pharmacotherapy selection70, 71. For example, in a sample of 318 patients, the diagnosis of PTSD was not associated with the prescription of any specific medication class, while symptom clusters were: anticonvulsant prescription was linked to avoidance symptoms, antidepressant prescription to numbing symptoms, anxiolytic prescription to intrusions, and mood stabilizer prescription to hyperarousal71. Similarly, in panic disorder, anxiolytics were more often prescribed for physical symptoms of the fear response, whereas antidepressants and anticonvulsants as well as anxiolytics were prescribed for psychological symptoms. A similar matching of medication class with symptom profile was found for agoraphobia (public vs. enclosure), OCD (cleaning, checking), social anxiety disorder (interactive vs. performance), and specific phobia (animal, situational, blood). Clearly, the symptom profile is guiding prescribers’ current pharmacotherapy choices, and the field of personalized medicine would be advanced by randomized controlled trials to validate (or not) such matching of symptom profile to medication.

The same argument holds for psychotherapy, which has been confounded by utilization of CBT packages that combine multiple therapeutic strategies (e.g., breathing retraining, cognitive restructuring, exposure therapy, response prevention). There have been calls to match the core active ingredients of these therapy packages to specific symptom profiles (e.g., breathing retraining to arousal regulation, cognitive restructuring to cognitive distortions, exposure therapy to avoidance)72, 73. This remains an important area of future research. Nonetheless, it is quite possible that the practicing clinician already tailors the core ingredients of CBT to symptom presentations, in the same way as observed for pharmacotherapies.

CLINICAL SUBTYPES

Each of the anxiety and related disorders is characterized by significant heterogeneity, and several clinical subtypes have been delineated. The content of the fear or anxiety (cognitive component), the physiological reactions (such as a panic attack), and the behavioral response (which often includes avoidance and may include safety behaviors) can be useful in determining whether or not a distinctive clinical subtype is present. In addition, a range of other approaches to subtyping have been taken, including those based on age of onset and on comorbid symptoms. Here we consider the main clinical subtypes that have been posited for key anxiety and related disorders.

In GAD, it is useful to assess both the nature of the worries, as well as the range of psychic (psychological) versus somatic (physical) symptoms. The worries may focus on death (e.g., someone not calling when he said he would means he has died), disease (e.g., “headache means I have a brain tumor”), destruction (e.g., “the leak in the ceiling means I need a new roof and if I don’t get it in time my house will be ruined”), and sometimes destitution (e.g., “If I lend my sister the money, she will never stop asking and I'll end up broke”). Tools such as the Penn State Worry Questionnaire53 assess the range and focus of GAD worries, while the psychic and somatic subscales of the Hamilton Anxiety Rating Scale (HAM-A)74 are useful for assessing the range of symptoms.

Knowing the precise nature of the worries is important for CBT, which may focus on cognitive restructuring of particular worries or exposure for particular kinds of fears. In terms of pharmacotherapy, an early suggestion was that tricyclic antidepressants are more useful for psychic symptoms, while benzodiazepines are more useful for somatic symptoms75. However, there has been relatively little subsequent evidence to support the selective response of psychic and somatic symptoms to different pharmacotherapies. A range of medications that are efficacious for GAD improve both psychic and somatic symptoms76-79.

Concerning OCD, a substantial literature has emphasized that obsessions and compulsions tend to fall on a few symptom dimensions, including washing, checking, symmetry and hoarding80. Although many patients have symptoms that lie on different dimensions, or experience a range of symptoms from different dimensions over time, there is some evidence that symptom dimensions are associated with particular psychobiological characteristics and treatment outcomes. In particular, hoarding symptoms are less likely to respond to SSRIs. Further work is needed to determine whether patients with hoarding symptoms who do not respond to SSRIs may respond to augmentation with dopamine antagonists81.

Insight in OCD can be ascertained by questioning the patient about the consequences of not engaging in the compulsions and the likelihood that the feared consequences will actually occur. It may be helpful to ask the patient if the feared consequences would be likely to occur for someone else, in order to assess their thought process without the influence of their own anxiety about not performing the compulsions. Insight in OCD can be formally assessed with measures such as the Brown Assessment of Beliefs Scale82. OCD patients with poor insight may be less likely to access or respond to pharmacotherapy and psychotherapy83. Such patients may require additional interventions such as family-based treatments84 and adjunctive dopamine antagonists85.

If OCD patients have current or past tics, it is important to determine if the compulsions are more tic-like (e.g., throat-clearing) or aimed to reduce anxiety (e.g., handwashing after feeling contaminated). Tic-related OCD is marked by a number of features, including early onset, male predominance, family history of tics, and more often having symptoms that involve responding to an urge (or premonitory sensory symptoms) or having to feel “just right”. Tic severity may be formally assessed with a number of measures86. Tic-like compulsions do not respond well to exposure and response prevention, and may respond better to augmentation with dopamine antagonists83.

A range of other subtypes of OCD has been proposed, including early onset OCD83. While such work has been valuable to better understand the heterogeneity of OCD, there is insufficient treatment evidence for such subtyping to have clinical utility.

Concerning panic disorder, a number of different sets of pan­ic symptoms have been found to cluster together, including respiratory, nocturnal, non-fearful, cognitive and vestibular symptoms31. Investigation of the respiratory physiology in panic disorder has been particularly useful in advancing understanding of the neurobiology of the condition87. Nevertheless, there is no strong evidence to indicate that any of these subtypes has a distinctive psychobiology, nor is there good evidence that any has a selective treatment response88. It is possible, however, that more extensive study will lead to more specific treatment recommendations for panic disorder subtypes.

PTSD is diagnosed in the DSM-5 using twenty symptoms that fall in four symptom subgroups, namely intrusions (five symptoms), avoidance (two symptoms), negative alterations in cognition and mood (seven symptoms), and arousal (six symptoms). While it has long been suggested that different symptom dimensions of PTSD are underpinned by different neurobiological mechanisms89, 90, it seems that there are strong genetic correlations across PTSD symptom dimensions and that efficacious pharmacotherapy for PTSD reduces symptoms across dimensions91. As noted earlier, the prescription of anticonvulsants has been linked to avoidance, that of antidepressants to numbing symptoms, that of anxiolytics to intrusions, and that of mood stabilizers to hyperarousal71, but further work is needed to provide the evidence base for such decision-making.

It has been hypothesized that there is a dissociative subtype of PTSD, with a distinctive neurobiology92. This subtype may be characterized by overmodulation of affect, rather than undermodulation of affect with re-experiencing and hyperarousal symptoms. Most clinicians assess dissociation via psychiatric history, but it may be useful to employ a formal tool such as the Dissociative Experiences Scale (DES)93. The DES-II is a 28-item self-report measure that assesses the frequency of dissociative experiences through daily life, with scores over 30 considered high94.

Recording treatment sessions for later review may be helpful for patients with dissociation symptoms, as well as frequent grounding, breaks, and progressing more slowly with traumatic content in order to not overwhelm the patient. Further, in keeping with the hypothesis that dissociation is linked to avoidance, there is evidence that cognitive processing therapy should include an exposure component when dissociation is present95. The ICD-11 construct of “complex PTSD” is marked by increased levels of early childhood trauma and dissociative symptoms, but further work is needed to determine what specific interventions would improve outcomes in this condition96.

The DSM-IV included a “generalized” specifier for social anxiety disorder, referring to patients with a broader range of social fears. In the DSM-5, this has been replaced by a “performance only” specifier, which is used when the fear is limited to speaking or performing in public. There is a view that social anxiety disorder ranges from single fears through to multiple fears, and that patients with more fears have greater severity and impairment97. There is some evidence that patients with “performance only” social anxiety disorder may respond to beta-adrenergic blockers (such as propranolol or atenolol)98. SSRIs, on the other hand, may be useful for patients with both more limited or more generalized social anxiety disorder99. CBT seems to be effective for all types of social anxiety.

Specific phobias include an animal type (e.g., spiders, insects, dogs), a blood-injection-injury type (e.g., needles, invasive medical procedures), a natural environment type (e.g., heights, storms, water), a situational type (e.g., airplanes, elevators, enclosed places) and “other” types (e.g., phobic avoidance of situations that may lead to choking, vomiting, or contracting an illness). Exposure techniques tailored to particular phobias are helpful for this range of specific phobia types.

The blood-injection-injury type, in contrast to other phobias which result in persistent tachycardia in response to feared cues, may be characterized in some patients by a diphasic response, with an initial rise in heart rate followed by vasovagal bradycardia and, in some cases, syncope100, 101. If patients faint upon exposure to cues, exposure therapy can be conducted with the patient lying down. It may be useful to teach patients an isometric muscle tensing technique that can help increase blood pressure during exposure to feared cues102.

The situational type of specific phobia often overlaps with agoraphobia and/or panic disorder and therefore typically requires cognitive techniques in addition to exposure.

SEVERITY

Assessing the severity of anxiety symptoms is an important component of the evaluation of the patient with an anxiety or related condition.

The DSM-5 includes symptom severity measures for each of the anxiety and related disorders, and several standardized symptom measures are widely used in clinical practice and research. These include the GAD-738 and the Penn State Worry Questionnaire53 for GAD; the Y-BOCS54 for OCD; the Panic Disorder Severity Scale57 and the Panic and Agoraphobia Scale58 for panic disorder; the Mobility Inventory for Agoraphobia56 and the Albany Panic and Phobia Questionnaire-Agoraphobia55 for agoraphobia; the PCL-559 and the CAPS-560 for PTSD; the Fear Survey Schedule63 for specific phobia; and the Social Phobia and Anxiety Inventory61 and the Liebowitz Social Anxiety Scale62 for social phobia (see Table 2).

Table 2. Tools to assess severity of anxiety and related disorders Agoraphobia

Albany Panic and Phobia

Questionnaire-Agoraphobia55

Number of items: 27

Scale: 0-8

Subscales: 9

Mobility Inventory for Agoraphobia56

Number of items: 26

Scale: 0-5

DSM-5 severity measure44, 47

Number of items: 10

Scale: 0-4

Generalized anxiety disorder

Generalized Anxiety Disorder-7 (GAD-7)38

Number of items: 7

Scale: 0-3

Penn State Worry Questionnaire53

Number of items: 16

Scale: 1-5

DSM-5 severity measure44, 46

Number of items: 10

Scale: 0-4

Obsessive-compulsive disorder

Yale-Brown Obsessive Compulsive Scale (Y-BOCS)54

Number of items: 10

Scale: 0-4

Subscales: 2

DSM-5 severity measure44, 48

Number of items: 10

Scale: 0-4

Panic disorder