THE NEUROSCIENTIFIC BASIS OF EVIDENCE-BASED TREATMENTS FOR PTSD – A SELECTIVE REVIEW
Journal Title: Праці Наукового товариства ім. Шевченка - Year 2017, Vol 49, Issue
Abstract
Posttraumatic Stress Disorder (PTSD) includes a) exposure to a signifi cant traumatic event, b) intrusive recollections, c) avoidant symptoms d) increased physiological arousal or amnesia for the traumatic event). While up to 90% of the US adult civilian population has a lifetime exposure to at least one signifi cant traumatic event, only 8-10% develop PTSD. While PTSD can result in signifi cant morbidity and dysfunction, evidence-based treatments can now be matched with an emerging understanding of underlying neurobiology. Meta-analysis demonstrates that certain selective serotonin reuptake inhibitors (SSRIs) and serotonin and norepinephrine reuptake inhibitors (SNRIs) are superior to placebo in attenuating PTSD symptoms. Unfortunately, the effect size is small (0.23), side-effects are common and these drugs may be less effi cacious when PTSD results from combat trauma rather than from civilian trauma. Recurring nightmares of the triggering event contribute to the sleep disturbances that affect some 70% of patients with PTSD. Although available data unequivocally support the effi cacy (effect size ~ 1.0) of prazosin, an α1-adrenergic receptor antagonist, it remains underutilized in most clinical settings. Patients with PTSD are more sensitive to the anxiogenic effects of an intravenously administered 5HT2C agonist or an adrenergic α2 receptor antagonist. This suggests that SSRIs and SNRIs may act by downregulation hypersensitive 5HT2C receptors. Analogously, since presynaptic α2 receptors are inhibitory to effl ux of noradrenaline, symptoms of PTSD could be mediated by excessive stimulation of postsynaptic α1 receptors. Prazosin may act to attenuate this stimulation. Brain regions involved in modulation of emotion, such as the dorsal and rostral anterior cingulate cortices, as well as the ventromedial prefrontal cortex show decreased activity in PTSD, resulting in excessive input from the amygdala, an evolutionarily older brain region dominant in threat responses. Thus, PTSD can be conceptualized as a dysregulation of brain circuits that integrate historical information of a traumatic event (memory) and autonomic responses. Fortunately, memory storage is not a onetime event but a process repeated with each use of that memory. Retrieval of a memory renders it temporarily available for modifi cation at the cellular and systems level. This principle is thought to underlie several independently developed psychotherapeutic approaches. The observation that recurring, disturbing thoughts of PTSD could be permanently abolished, if the subject’s eyes were automatically moving in a multi-saccadic manner while the disturbing thought was being held in consciousness, catalyzed the development of Eye movement desensitization and reprocessing therapy (EMDR). Analogous neurobiological mechanisms are likely operative in other trauma focused cognitive behavioral therapies (TFCBTs). Indeed, the favorable side effect profi le and relatively large effect sizes (~ 1.0) of EMDR and TFCBTs have led to their designation as fi rst line treatments for PTSD, ahead of pharmacological approaches. Available studies show that EMDR and TFCBTs affect memory-driven activation of cortical regions implicated in emotional processing, including the amygdala. Neuroscience provides a mechanistic explanation for current, evidence-based treatments for PTSD and promises to facilitate developments of additional treatment approaches. Such somatic and psychotherapeutic modalities should be considered part of a balanced, biopsychosocial approach to recovery and rehabilitation for individuals with PTSD.
Authors and Affiliations
George Jaskiw
Keywords
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