Anxiety Disorders ____________________________________________________________________________
in therapy and the availability of well-trained therapists. Phar- macotherapy is also considered a first-line treatment option for anxiety disorders. While many medications have received FDA approval to treat anxiety, antidepressants have proven to be the most effective. Either a selective serotonin reuptake inhibitor (SSRI) or serotonin-norepinephrine reuptake inhibitor (SNRI) is recommended initial treatment of GAD, SAD, and panic disorder [350]. Benzodiazepines, which once served as a first- line option, are now best reserved for short-term use or as a supplement to the primary treatment regimen. Advances in anxiety disorder neuroscience have increasingly pointed to the necessary role of fear extinction learning (through exposure therapy) in addressing underlying patho- physiology. While efficacy is shown with CBT and exposure, patients can have difficulty with the demanding and exhaust- ing therapy process, and many who do manage to complete therapy respond partially and relapse with time. Efforts to improve CBT/exposure outcomes have led to the investigation of augmenting agents. In contrast to standard anti-anxiety drugs, these agents are not anxiolytic but are used to promote and accelerate long-term adaptive changes in brain function initiated by successful exposures [137]. Any review of treatment efficacy for anxiety disorders, and pharmacotherapy in particular, requires a disclaimer. Most treatment outcomes were based on studies using methodolo- gies that excluded those with additional anxiety disorders and comorbid psychiatric or medical disorders. Patients seeking care for anxiety problems in primary care and other real-world settings often differ from carefully screened study participants. The extent that efficacy, response, and remission rates reported in the published research generalize to typically more complex clinic patients has been questioned [138]. Treatment refusal and attrition are significant problems. Patients with anxiety disorders show treatment refusal rates of 25% to 30% and treatment dropout rates of 10% to 82% [139]. Treatment dropout is very high in exposure therapy, as patients repeatedly confront (with graded intensity) the situations or objects that trigger their greatest fear or panic response. The intensity of distress during exposure can overwhelm patients, and with avoidance the hallmark feature of most anxiety disor- ders, attrition is significant [2; 139]. Attrition can interfere with evaluating treatment efficacy (or the lack thereof), and unless explicit in study reporting, can be misleading. Attrition is also a clear concern in the clinical care of patients with anxiety. PREDICTORS OF WORSE TREATMENT RESPONSE AND OUTCOMES SEPAD Severe forms of SEPAD are associated with a pervasive negative influence on treatment response. Comorbid SEPAD is highly correlated with poor treatment response and patient outcomes across a range of anxiety and mood disorders. SEPAD nega- tively impacts response to major depression treatment and is
linked to worse symptom chronicity and quality of life. SEPAD decreases CBT response and predicts worse outcomes in patients treated for panic disorder, GAD, or SAD. SEPAD also predicts nonresponse to selective serotonin re-uptake inhibitors (SSRIs) or tricyclic antidepressants (TCAs) in patients with panic disorder with agoraphobia [98; 140]. Chronic Pain Uncontrolled pain is also increasingly recognized to negatively impact anxiety disorder treatment outcomes. In primary care patients with a GAD or panic disorder diagnosis treated for severe anxiety and followed for one year, patients with mod- erate or greater pain levels were found to show significantly lower rates of clinical improvement [141]. A cohort of 1,122 individuals with remitted anxiety or depressive disorders were followed up to four years, and pain (but not chronic disease) was associated with recurrence during follow-up [142]. Social Drinking Problematic, excessive drinking clearly disrupts treatment response, but social drinking can also aggravate panic disorder and probably other anxiety syndromes. The short-acting effects of alcohol wear off rapidly, followed by rebound to a state of hyper-excitability that may be more problematic for patients with anxiety. This can occur with one to two drinks in some patients, who often do not even consider this a contributing factor to their anxiety complaint. Explaining the simple physiol- ogy of rebound excitation after profound neuronal inhibition will often convince patients that alcohol may be sensitizing the neural circuits subserving their anxiety and that a trial period of abstinence is indicated [28]. Other Anxiety Disorders Highly symptomatic panic inhibits benefit from interpersonal psychotherapy, either alone or combined with SSRIs. The pres- ence of any anxiety disorder impairs response to treatment of comorbid major depression [98]. Patients with major depressive disorder and a comorbid anxiety disorder demonstrate longer time to recovery and greater risk of early treatment termination. Patients with comorbid anxiety and depressive disorders gener- ally have worse outcomes than patients with either disorder alone. Patients with comorbid GAD and major depression are significantly more likely to remain symptomatic than those with depression or GAD alone [143]. When anxiety symptoms are present within a dominant depressive disorder, antidepressant drugs are often effective in reducing anxiety [144]. However, depression that follows or is comorbid with an anxiety disorder usually indicates greater severity and worse prognosis [145]. Among treatment-seeking patients with panic disorder, SAD, or GAD followed over two years, symptom changes in GAD were most specifically related to changes in impairment, suggesting that treatment of patients with multiple anxiety disorders should initially focus on GAD symptoms or employ trans-diagnostic modalities [146].
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