Anxiety Disorders ____________________________________________________________________________
Overlooked Diagnosis, Comorbid Conditions, or Psychosocial Contributors
• Side effects often precede therapeutic benefit and typically recede over time. • It is important to expect some discomfort prior to the benefit. • Successful treatment may involve dose adjustments and/or trials of different medications to maximize response and minimize side effects. • Most people must be on medication at least 6 to 12 months after adequate response, and patients may show improvement at two weeks but need a longer length of time to really see response and remission. • It is important to take the medication as prescribed, even after feeling better, because early discontinuation is associated with high rates of relapse/recurrence. • Do not stop taking the medication without calling the provider. • Side effects can often be managed by changing the dose or dosage schedule. A novel approach to improve patient understanding of their anxiety disorder and treatment rationale incorporates anxi- ety neuroscience. A core concept is that anxiety disorders/ symptoms with amygdala origin (e.g., panic disorder, phobias) require different approaches than anxiety of cortical origin (e.g., SAD, GAD). Educating patients of the brain-based source of their anxiety can improve treatment adherence and empower patients to modify these areas of brain function. For example, patients with cortex-related symptoms such as obsessions, perfectionism, and chronic worry benefit from an approach termed “Question Your Cortex.” They can be encouraged to identify anxiety-generating thoughts in the cor- tex and use cognitive restructuring methods to exploit cortical neuroplasticity by modifying their thoughts. However, cortex- based interventions are not effective at reducing or managing anxiety with amygdala-mediated symptoms; for these patients, exposure to feared situations is stressed. Most patients benefit from a combination of cortex- and amygdala-focused interven- tions, with the rationale and order of interventions differing by disorder and individual patient [247]. Antidepressant Withdrawal In reference to withdrawal of SSRI therapy, “withdrawal syn- drome” has been largely replaced by the term “discontinuation syndrome” with industry support to convey the message that SSRIs do not cause addiction, dependence, or withdrawal syndrome as one might experience following cessation of benzodiazepines. This has been challenged, given the poten- tial seriousness of SSRI post-cessation symptoms, as a false dichotomy that minimizes the vulnerabilities induced by SSRIs. For the purposes of this course, the term “withdrawal syndrome” will be used [248]. Clinicians should be aware of these withdrawal syndromes, as misdiagnosis may result in inappropriate diagnostic tests and treatment and unnecessary patient distress and morbidity [248].
When established that adequate treatment was delivered and received, factors contributing to treatment resistance can include misdiagnosis or overlooked comorbidities or psycho- social factors. The following should be revisited [28]: • Primary diagnosis accuracy • Presence and contribution of unrecognized substance use disorder, psychiatric comorbidity, and/or complicating medical condition • Psychosocial or lifestyle factors (e.g., caffeine overuse, sleep deprivation, interpersonal or family conflict) Necessary Treatment Duration for Evidence of Response or Dose Escalation Compared with treatment of simple depression, SSRI/SNRI treatment of anxiety disorder typically requires somewhat higher dosage and longer initial treatment duration before realizing a therapeutic effect. With duloxetine and escitalo- pram, a satisfactory response is unlikely without some degree of clinical benefit within four weeks of initiating therapy. With pregabalin, onset of clinical effect within two weeks is associ- ated with a 5.3-fold increased likelihood of treatment response; 25% of patients not showing clinical effect at two weeks will ultimately respond to treatment. A pregabalin dosage of 150 mg/day is suboptimal; a dose-response effect usually requires 300–600 mg/day [243]. In clinical trials of venlafaxine XR, therapeutic benefits usu- ally diverged from placebo at four to six weeks. However, the percentage remitted from panic disorder in one trial increased from 18% at 6 weeks to 50% at 12 weeks [244]. SSRIs/SNRIs usually take two to six weeks to show an initial “partial” response, often defined as ≥25% improvement (i.e., beyond random noise or natural symptom fluctuations). Full benefit may not appear for another four to six weeks or longer. Data from patients with depression, and some uncontrolled data with anxiety, suggest that about 20% of patients may need 10 to 12 weeks or longer before responding. Thus, dose escala- tion to highest level tolerated is recommended for patients with incomplete response before adequate time has passed [245]. In contrast to depression, antidepressant efficacy in anxiety disorders appears to be lost soon after stopping, with anxiety recurrence being the rule rather than the exception [228]. Patient Education Successful medication treatment often involves dosage adjust- ments and/or trials of a different medication at some point in order to maximize response and minimize side effects. Because patient adherence is the essential pre-condition for maximum clinical benefit, the following messages should be communicated to the patient to encourage and support ongo- ing medication adherence [246]:
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