Anxiety Disorders ____________________________________________________________________________
(before 12 exposures), and more than one to two hours before an exposure. Higher-dose DCS shows weaker NMDA partial agonist or antagonist effects. Key extinction learning processes occur hours following exposure, and DCS blood concentra- tion peaking at four to six hours makes it more effective taken within one to two hours before exposure for peak activity to coincide with key extinction processes. Repeated DCS use can desensitize the NMDA receptor complex, leading DCS to effectively work as an NMDA antagonist. Long-term anti- depressants can induce neurochemical changes at the glycine binding site of the NMDA receptor complex, which alters the action of DCS. Therefore, use of DCS should consider the narrow therapeutic window and the need to be administered without concomitant medication, acutely, and at low doses one to two hours pre-exposure [310]. DCS is associated with serious risks. DCS not only enhances cognitive processes during fear extinction learning but also during fear memory reconsolidation, thus improving good exposures and worsening bad exposures. If fear-inducing stimu- lus re-exposure during fear memory reactivation is too brief relative to the strength of fear conditioning or if fear decrease during exposure is inadequate, little extinction is induced and DCS can augment the process of fear memory reconsolidation to worsen symptoms [310]. These findings led to DCS administered post-exposure, con- tingent on the level of fear reduced (i.e., extinction learning achieved) by the end of the exposure session. Preliminary evidence shows that this approach may be effective in capital- izing on the benefits while minimizing the risks of DCS use to augment exposure therapy [310]. Yohimbine Hydrochloride Yohimbine hydrochloride (YOH) is a selective competitive alpha2-adrenergic receptor antagonist currently only approved for veterinary use. This compound increases extracellular norepinephrine in humans by blocking autoreceptor inhibi- tion of norepinephrine release. This mechanism potentially facilitates extinction learning in exposure therapies. Placebo- controlled trials have been performed in specific phobia and SAD. Subjects with claustrophobia given YOH 10.8 mg before two 60-minute exposures of sitting in a closed, dark chamber showed more robust reductions in claustrophobia symptoms. Patients with SAD given YOH 10.8 mg before four exposure sessions showed accelerated treatment improvement and lower levels of social anxiety symptoms. More research is needed, but these results suggest YOH may have a role in augmenting exposure therapy [164]. Glucocorticoids Glucocorticoids have shown enhancement of virtual reality- based exposure therapy for fear of heights and were investigated for possible outcome enhancement in exposure-based group therapy for spider phobia. In one randomized controlled trial, cortisol 20 mg or placebo was orally administered one hour before each therapy session and patients were assessed
at one-month post-therapy follow-up. Compared to placebo, cortisol led to significantly greater reduction in fear of spiders at follow-up but not immediately post-treatment, as measured psychometrically and by exposure to live spiders. Groups did not differ in phobia-unrelated state-anxiety before and after exposure sessions and at follow-up [314]. Another randomized controlled trial investigated the role of hydrocortisone as an adjunct to brief CBT for specific (spi- der) fear [315]. Spider-fearful participants were randomized to receive either 20 mg hydrocortisone or placebo one hour prior to single-session, predominantly computerized, exposure- based CBT. Participants’ fear of spiders was assessed using self-report and approach behaviors measured at baseline and at one-day and one-month follow-up. Threat processing was assessed at baseline and at one-day follow-up. Cortisol and cortisone levels from hair and saliva samples were analyzed at baseline. All measures improved following CBT. Augmenta- tion with hydrocortisone resulted in greater improvement in self-reported fear and approach behavior but not threat bias. Neither threat bias nor endogenous glucocorticoids predicted symptom change. Evidence indicates that higher hair cortisone predicts a stronger threat bias reduction [315]. Methylene Blue Methylene blue is a nitric oxide synthase inhibitor, central MAO inhibitor, and cerebral metabolic enhancer. A placebo- controlled trial of subjects with severe claustrophobic fear found that participants displaying low fear at the end of extinction training showed significantly less fear at follow-up if they received methylene blue post-training relative to placebo. In contrast, participants displaying moderate-to-high levels of post-training fear tended to fare worse at follow-up with methylene blue compared with placebo. Similar to the profile of DCS, methylene blue enhanced memory and retention of fear extinction when administered after a successful exposure session, but it may have deleterious effects on extinction when administered after an unsuccessful session [316].
CAPNOMETRY-ASSISTED RESPIRATORY TRAINING
Panic disorder and sensitivity to increased carbon dioxide (CO 2 ) levels common in patients with panic disorder may represent pathologically amplified survival mechanisms. Panic disorder reflects a “fight-or-flight” response, and CO 2 hypersen- sitivity is an evolutionary carry-over from when alarm response to dwindling oxygen helped ensure survival. Panic attacks that awaken people at night only occur during non-REM sleep, when deep relaxation and slowed breathing lead to rising CO 2 levels that trigger a false suffocation alarm [317]. Capnometry-assisted respiratory training (CART) is an inter- vention that addresses CO 2 fluctuation and its role in panic attacks for some people. CART targets respiratory dysregula- tion and hypocapnia through a four-week training using imme- diate feedback of end-tidal CO 2 pressure (PCO 2 ). Patients are taught how to raise subnormal PCO 2 levels (caused by hyper-
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