There is evidence relating Cannabis use in PTSD patients to relaxation, sleep improvement, attenuation of hyperarousal and anxiety, and reduced values in the Clinician Administered Posttraumatic Scale (CAPS).
Similarly, the results of open-label, populational, and double-blind placebo-controlled studies have shown the benefits of using Δ9-tetrahydrocannabinol (THC), its synthetic version dronabinol or its analog nabilone to manage insomnia and nightmares in PTSD patients. However, contradictory results have also been reported, leading some authors to question the value of this Cannabis-based approach. Differences in dose, route of administration, treatment regimen, level of THC tolerance, and current and past stress may account for the mixed findings above-mentioned. Of note, the potential effects of THC/dronabinol or nabilone on aversive memory extinction and reconsolidation are under investigation.
In contrast, it is still unknown whether cannabidiol (CBD), the main compound of Cannabis devoid of psychotomimetic effects, can impair the reconsolidation of aversive memories and facilitate their extinction in humans, although its anxiolytic action has already been reported. Similarly, associating THC with CBD could be therapeutically advantageous, but studies focusing on extinction or reconsolidation of aversive/traumatic memories are still incipient.
Fear extinction is a form of inhibitory learning that suppresses the expression of the original aversive/traumatic memory. As a consequence, individuals express less fear responses. In both laboratory animals and healthy humans, prolonged and repeated exposures to conditioned cues without presenting the aversive stimulus can induce it. Preclinical studies have shown that the extinction process requires activity and plasticity in several interconnected brain regions, including the infralimbic and prelimbic subregions of the medial prefrontal cortex [homologous to the human ventromedial prefrontal (vmPFC) and dorsal anterior cingulate (dACC) cortices, respectively], and some amygdala nuclei. Specific PTSD psychotherapies (e.g., prolonged exposure therapy) are based on extinction learning. Patients suffering from this psychiatric condition, however, often present extinction impairments accompanied by a hypoactive vmPFC, hyperactive dACC and amygdala, and a smaller and hypofunctional hippocampus. The abnormal functioning of these brain regions could explain not only the hyperarousal and extinction deficits but also the increased responsiveness to trauma-unrelated stimuli leading to fear overgeneralization. Noteworthy, over time, the original aversive/traumatic memory can spontaneously reemerge, which also limits the efficacy of the extinction approach.
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