AI Article Synopsis
- The study investigates the potential of aprepitant, an NK1 receptor antagonist, to treat patients with comorbid PTSD and alcoholism, as both conditions may share underlying neural mechanisms.
- Fifty-three patients were involved in a 4-week double-blind trial to compare the effects of aprepitant versus a placebo on PTSD symptoms and reactions to stress and alcohol-related cues.
- Although aprepitant did not improve PTSD symptoms or stress reactions, it increased fMRI activity in the ventromedial prefrontal cortex during negative stimuli, suggesting it might aid in enhancing therapies aimed at extinguishing fear responses and reducing alcohol cravings.
Article Abstract
Rationale: Posttraumatic stress disorder (PTSD) and alcoholism are frequently comorbid, suggesting the possibility of overlapping neural substrates. The neurokinin 1 (NK1) receptor for substance P (SP) has been implicated in both stress- and alcohol-related behaviors. The NK1 antagonist aprepitant, clinically available as a treatment for chemotherapy-induced nausea, offers a tool to probe a potential role of the SP/NK1 system in comorbid PTSD and alcoholism.
Objectives: The aim of this study is to evaluate the efficacy of aprepitant for treatment of comorbid PTSD and alcoholism.
Methods: Fifty-three patients with PTSD and alcoholism were admitted for 4 weeks to an inpatient unit at the NIH Clinical Center and randomized to double-blind aprepitant (125 mg/day; based on PET studies reporting >90 % central receptor occupancy at this dose) or placebo. After reaching steady state, subjects were assessed for PTSD symptom severity, behavioral and neuroendocrine responses to stress and alcohol cues, and functional magnetic resonance imaging (fMRI) responses to stimuli with positive or negative emotional valence.
Results: Aprepitant treatment had no effect on PTSD symptoms or subjective or physiological responses to stress or alcohol cues. However, aprepitant robustly potentiated ventromedial prefrontal cortex (mPFC) fMRI responses to aversive visual stimuli.
Conclusions: Despite the lack of effect on PTSD symptoms and responses to stress/alcohol cues, NK1 antagonism activated the ventral mPFC, an area considered hypoactive in PTSD, during exposure to aversive stimuli. Because this brain area is critically important for extinction of fear memories and in alcohol craving and relapse, our finding suggests that NK1 antagonism might be a useful pharmacological treatment to enhance extinction-based cue-exposure therapies.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4512162 | PMC |
| http://dx.doi.org/10.1007/s00213-014-3665-4 | DOI Listing |
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