Anxiety Disorders ____________________________________________________________________________
SOCIAL ANXIETY DISORDER Patients with SAD have shown hyper(re)active limbic, frontal, and parietal brain regions involved in emotional and atten- tional processes. Compared to healthy subjects, patients with SAD display increased cortical thickness in frontal, parietal, and other brain areas. CBT treatment success and symptom improvement have been associated with changes in prefrontal regions involved in emotion regulation [87]. Persons with SAD and GAD share core features of persistent, debilitating focus on negative or potentially threatening experi- ence. This negative affective bias is characterized by increased threat processing at the neural, psychologic, and behavioral levels, with engagement of the dorsal medial prefrontal cortex- amygdala circuit during aversive processing. Anxiety disorder subtypes frequently co-occur, and while abnormal activation of this neural circuitry that mediates bias toward threats is diagnosis-independent, it also represents a cardinal feature of SAD and GAD [88]. SAD pathophysiology includes heightened autonomic arousal to social cues and novelty. Fear processing appears medi- ated by the amygdala, in which neuroimaging studies show exaggerated activations with exposure to novel facial stimuli. Amygdala activation to novelty is also found in persons with a behavioral inhibition temperament. Other pathophysiologic models suggest that exaggerated hypothalamic-pituitary-adrenal axis reactivity to environmental stimuli may be involved in SAD [89; 90; 91; 92]. SPECIFIC PHOBIA Amygdala, anterior cingulate cortex, and insula hyperactivity is believed to be the underlying pathophysiology of specific phobia. Neuroimaging studies have shown increased amyg- dala activation with exposure to phobic-relevant cues, and heightened activity in thalamic, insula, and dorsal anterior cingulate cortex regions [93; 94; 95]. Meta-analyses suggest the left amygdala/globus pallidus, left insula, right thalamus, and cerebellum regions are all more active among patients with a phobia compared with controls when exposed to phobic-relevant stimuli. Acute, exaggerated parasympathetic nervous system activity with exposure to stimuli is thought to underlie the vasovagal syncope experienced by up to 80% of people with blood-injection-injury phobia [96]. Exposure-based therapy leads to deactivation in the right frontal cortex, limbic cortex, basal ganglia, and cerebellum, and increased activity in the thalamus [97]. ADULT SEPARATION ANXIETY DISORDER SEPAD etiology is thought to arise during childhood by disrupted caregiving environments that promote greater hypothalamic/pituitary stress responsivity. Neuroimaging research has focused on brain circuitry that shows abnor- mal activity at single time points during anxiety from close attachments. The underlying neural circuitry that mediates separation-hypersensitive attachment includes subcortical areas (amygdala, hippocampus, striatum) and cortical limbic areas
(insula, cingulate). Predisposing endophenotypes may interact with circuitry involved in attention, learning, and executive control (medial prefrontal cortex, superior temporal sulcus, and temporoparietal junction). With social interaction central to separation anxiety, neural circuitry involved in separation- sensitive social representations that predict danger when separation occurs may include the anterior temporal cortex [98]. SEPAD is associated with hypersensitivity to inhaled carbon dioxide, with a similar pattern to patients with panic disorder, suggesting SEPAD and panic disorder may share a common pathophysiologic basis [99; 100]. CLINICAL AND DIAGNOSTIC FEATURES As with other psychiatric disorders, the treatment of anxiety disorders is guided by conceptualization of the disorder and theoretical basis for disorder/treatment relationships. The understanding of anxiety disorders has changed over time with input of new evidence. In the United States, the DSM, published by the American Psychiatric Association, is the authoritative reference in defining and diagnosing psychiatric disorders. In the modern era, revised DSM editions have been published in 1980, 1994, 2000, and most recently in 2013 with the DSM-5. To better reflect current thinking on anxiety disorders, the DSM-5 made several important changes from the 1994 DSM- IV and its 2000 text revision [32; 101]. As noted, the chapter on anxiety disorders no longer includes OCD, PTSD, and acute stress disorder. New sections were added for these conditions: obsessive-compulsive and related disorders and trauma- and stressor-related disorders. Duration criteria for several anxiety disorders were extended to six months or longer to minimize overdiagnosis of transient symptoms, applied to all ages. With agoraphobia, specific phobia, and SAD, the requirement that patients recognize their anxiety as excessive or unreason- able has been eliminated. This change was based on evidence that individuals with such disorders often overestimated the danger in “phobic” situations and that older individuals often misattributed “phobic” fears to aging. Instead, the anxiety must be out of proportion to the actual situational danger or threat, with consideration of cultural contextual factors [102]. The DSM-5 (and previous DSM editions) has been criticized for emphasis on reliability at the expense of diagnostic valid- ity and for use of symptom-based diagnosis when symptoms alone may not best inform treatment selection. In response, the National Institute of Mental Health is developing the Research Domain Criteria, a new taxonomy for mental disorders that draws from genetics, neuroscience, and behavioral science [103]. Additionally, the DSM-5-TR, which was released in March 2022, includes the addition of prolonged grief disorder; the inclusion of symptom codes for suicidal behavior and non- suicidal self-injury; refinement of criteria; and comprehensive literature-based updates to the text [104].
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