____________________________________________________________________________ Anxiety Disorders
ventilation) to control dysfunctional respiratory patterns and related panic symptoms of shortness of breath and dizziness. CART uses novel technologies that allow precise assessment and monitoring of core respiratory variables. A portable cap- nometer offers breath-by-breath feedback of expired CO 2 and breathing rate, as measured via nasal cannula. In one study, four weeks of CART led to reductions in panic symptom severity and frequency comparable to standard CBT, maintained at 12-month follow-up. Patients with panic disorder/agoraphobia randomized to four weeks of CART or cognitive therapy showed significant and comparable reduc- tions in panic symptom severity and panic-related cognitions [281]. Across studies in patients with panic disorder with agoraphobia and asthma, compliance with the 17-minute, twice-daily exercises was high, and compliance correlated with the extent of panic symptom reduction [281; 318]. Changes in PCO 2 mediated and preceded changes in fear of panic sensa- tions, cognitive reappraisal of symptoms, and perceived control. Reductions in respiration rate were unrelated to outcome [281; 319]. These findings strengthen the idea that panic symptom reduction can be achieved through different mechanisms [162]. NEUROMODULATION THERAPIES Brain stimulation (also referred to as neuromodulation, neurostimulation, or somatic therapy) for the treatment of neuropsychiatric disorders was developed as an option for patients with severe disorders refractory to multiple treatments. Electroconvulsive therapy, introduced more than 75 years ago, has been historically the only widely used somatic treatment of psychiatric disorders. This was changed by the development and FDA approval of several minimally or non-invasive brain stimulation modalities with much greater specificity than elec- troconvulsive therapy. Other modalities are undergoing evalua- tion and possible market entry [320]. This approach shifts the treatment focus from altering synaptic neurotransmission to altering or modulating the function of entire neural circuits, the dysfunction of which underlies anxiety disorders [120]. Repetitive Transcranial Magnetic Stimulation The most studied neurostimulation approach in the United States is repetitive transcranial magnetic stimulation (rTMS). As discussed, patients with panic disorder often lack response or only partially respond to drug or psychologic treatments, which increases the risk of the disorder becoming chronic and disabling. Transcranial magnetic stimulation delivers non-invasive stimulation to the cerebral cortex, with currents induced by powerful, extremely brief magnetic fields. Admin- istration in a rhythmic, repetitive form is rTMS. Modulation of cortical excitability uses high-frequency rTMS to increase cortical excitability or low-frequency rTMS to inhibit cortical excitability of targeted areas. rTMS can also affect remote brain areas connected to the stimulated site [321].
Early studies of rTMS in anxiety disorders often found no dif- ference between active vs. sham rTMS, reflecting the inability to stimulate brain regions deeper than superficial cortical layers and inadequate treatment duration or post-treatment follow- up [322]. Subsequent technical refinements show treatment efficacy. A randomized controlled trial treated 28 patients with panic disorder and major depression with active or sham rTMS to the right dorsolateral prefrontal cortex. Response was defined as reduction by ≥40% in panic disorder severity and ≥50% in depression ratings. After four weeks, panic disorder response rate was 50% with active and 8% with sham rTMS, with no difference in depression. After eight weeks of active rTMS, response rates were 67% for panic and 50% for depressive symptoms. Significant improvements occurred in panic disor- der, major depression, clinical global impression, and social adjustment. Clinical improvements were maintained at six months post-treatment. While four weeks of rTMS was suf- ficient to significantly reduce panic symptoms, a longer course led to better outcomes for both panic disorder and major depression. These data suggest that inhibitory rTMS to the right dorsolateral prefrontal cortex affects symptom expression in comorbid anxiety and depressive disorder [323]. Another study found that inhibitory rTMS to the left dorsolateral prefrontal cortex showed therapeutic effects in patients with major depressive disorder [324].
NEW OR NOVEL ANXIOLYTIC AGENTS Cannabidiol
Cannabidiol is the second most abundant cannabinoid in Cannabis plants and lacks the consciousness-altering effects of delta-9-tetrahydrocannabinol (THC), the primary psychoactive compound in Cannabis. Cannabidiol is a pharmacologically broad-spectrum drug that has drawn increasing interest as a treatment for a range of neuropsychiatric conditions, including anxiety disorders. Preclinical evidence supports cannabidiol as a treatment for GAD, panic disorder, SAD, OCD, and PTSD when administered acutely, but few studies have investigated chronic cannabidiol dosing. Randomized controlled trials showed that, relative to placebo, cannabidiol significantly reduced anxiety in patients with SAD and GAD [136; 325]. In a series of randomized controlled trials using fear-condi- tioning paradigms, subjects who received cannabidiol (vs. placebo) all showed successful conditioning, extinction, and recall. When given after resolution of symptoms, cannabidiol enhanced consolidation of extinction learning. Cannabidiol administered pre- or post-extinction reduced the reinstate- ment of autonomic contextual responding. No acute effects of cannabidiol were found on extinction. These results are the first evidence that cannabidiol may enhance consolidation of extinction learning in humans, suggesting cannabidiol may have potential as an adjunct to extinction therapies for anxiety disorders [326].
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