Background: Eye movement desensitization and reprocessing [EMDR] is an innovative, evidence-based and effective psychotherapy for post-traumatic stress disorder [PTSD]. As with other psychotherapies, the effectiveness of EMDR contrasts with a limited knowledge of its underlying mechanism of action. In its relatively short life as a therapeutic option, EMDR has not been without controversy, in particular regarding the role of the bilateral stimulation as an active component of the therapy. The high prevalence of EMDR in clinical practice and the dramatic increase in EMDR research in recent years, with more than 26 randomized controlled trials published to date, highlight the need for a better understanding of its mechanism of action. Methods: We conducted a thorough systematic search of studies published until January 2018, using PubMed, ScienceDirect, Web of Knowledge and Scopus databases that examined the mechanism of action of EMDR or provided conclusions within the framework of current theoretical models of EMDR functioning. Results: Eighty-seven studies were selected for review and classified into three overarching models; (i) psychological models (ii) psychophysiological models and (iii) neurobiological models. The evidence available from each study was analyzed and discussed. Results demonstrated a reasonable empirical support for the working memory hypothesis and for the physiological changes associated with successful EMDR therapy. Recently, more sophisticated structural and functional neuroimaging studies using high resolution structural and temporal techniques are starting to provide preliminary evidence into the neuronal correlates before, during and after EMDR therapy. Discussion: Despite the increasing number of studies that published in recent years, the research into the mechanisms underlying EMDR therapy is still in its infancy. Studies in well-defined clinical and non-clinical populations, larger sample sizes and tighter methodological control are further needed in order to establish firm conclusions.

Background: Eye Movement Desensitization and Reprocessing (EMDR) is a psychotherapeutic approach that has demonstrated efficacy in the treatment of Posttraumatic Stress Disorder (PTSD) through several randomized controlled trials (RCT). Solid evidence shows that traumatic events can contribute to the onset of severe mental disorders and can worsen their prognosis. The aim of this systematic review is to summarize the most important findings from RCT conducted in the treatment of comorbid traumatic events in psychosis, bipolar disorder, unipolar depression, anxiety disorders, substance use disorders and chronic back pain. Methods: Using PubMed, ScienceDirect and Scopus, we conducted a systematic literature search of RCT studies published up to December 2016 that used EMDR in the mentioned psychiatric conditions. Results: RCT are still scarce in these comorbid conditions but the available evidence suggests that EMDR improves trauma-associated symptoms and has a minor effect on the primary disorders by reaching partial symptomatic improvement. Conclusions: EMDR could be a useful psychotherapy to treat trauma-associated symptoms in patients with comorbid psychiatric disorders. Preliminary evidence also suggests that EMDR therapy might be useful to improve psychotic or affective symptoms and could be an add-on treatment in chronic pain conditions.

The pathophysiology underlying the involuntary tics of Gilles de la Tourette syndrome (GTS) remains unknown. Here we used transcranial magnetic stimulation (TMS) to examine the excitability of two different inhibitory systems in the human motor cortex: short interval intracortical inhibition (SICI) and short interval afferent inhibition (SAI) in 10 healthy non-smoking controls and eight untreated non-smoking patients with GTS. Compared with the healthy control group, both SICI (measured at a range of conditioning intensities) and SAI were reduced in patients. This is consistent with the suggestion that reduced excitability of cortical inhibition is one factor that contributes to the difficulty that patients have in suppressing involuntary tics. In addition, the reduced SAI indicates that impaired intracortical inhibition may not be limited to the motor cortex but also involves circuits linking sensory input and motor output. A single dose of nicotine reduced tic severity as assessed by blind video scoring in the majority of patients. In addition, it abolished the difference between patients and controls in SICI and SAI. There was no effect of nicotine, and no difference between controls and patients in measures of motor or SICI threshold. This indicates that cholinergic input can modulate the efficiency of SICI and SAI differently in GTS and healthy controls.