Converging lines of evidence have implicated the amygdala in the pathophysiology of posttraumatic stress disorder. The primary purpose of our study is to assess the effect of propanolol, a beta adrenergic antagonism, on amygdala activation during a symptom provocation state in traumatized subjects with and without posttraumatic stress disorder.
Post-traumatic stress disorder (PTSD) is a type of anxiety disorder that's triggered by an extremely traumatic event. Traumatic events that may trigger PTSD include violent personal assaults, accidents, natural or human-caused disasters, or military combat. Converging lines of evidence have implicated the amygdala in the pathophysiology of posttraumatic stress disorder. Initially based on animal studies, the idea that memory for emotional material in humans is modulated by the noradrenergic system and by the amygdala, has received a strong support over the last decade. Evidence mainly comes from studies investigating the effect of emotion on encoding processes (Mc GAUGH, 2000). In that view, propranolol has been used somewhat successfully shortly after trauma to reduce the development of PTSD symptoms (Pitman et al., 2002; VAIVA et al., 2003). As already mentioned, "reconsolidation" studies developed in rats provide treatment strategies that can be used long after PTSD induction. Recent evidence indicates that consolidated long-term memory in human can also be influenced by events delivered after memory reactivation (Walker et al., 2003; HUPBACH et al., 2007), suggesting that human memory can be retroactively altered by treatments delivered in conjunction with memory reactivation. This seems to be confirmed by an as yet unpublished human based study that suggests that propranolol may impair reconsolidation of conditioned fear-response (Miller et al., 2004) The primary purpose of our study is to assess the effect of propanolol, a beta adrenergic antagonism, on amygdala activation during a symptom provocation state in traumatized subjects with and without posttraumatic stress disorder. One Functional magnetic resonance imaging (fMRI) will be performed (week 1) in 32 patients with PTSD and 32 controls (exposure to a traumatic event without PTSD) to examine amygdala activation during a provocation state. One half of the patients with PTSD and one half of the controls will receive propranolol prior the fMRI under double blind condition. In addition, a cognitive test battery will be performed (screening, week 0, 1, 2) before the fRMI acquisition and at follow up visits.
Study Type
INTERVENTIONAL
Allocation
RANDOMIZED
Purpose
TREATMENT
Masking
QUADRUPLE
Enrollment
5
A grip of 2 tablets of 20 mg each took 90 min before the emotional memory reactivation and the anatomical and functional exploration in fMRI
A grip of 2 tablets of 20 mg each took 90 min before the emotional memory reactivation and the anatomical and functional exploration in fMRI
A grip of 2 tablets of 20 mg each took 90 min before the emotional memory reactivation and the anatomical and functional exploration in fMRI
Saint-Antoine Hospital, Psychiatriy unit
Paris, Île-de-France Region, France
Effect of propanolol, a beta adrenergic antagonism, on amygdala activation during a symptom provocation state in traumatized subjects with and without posttraumatic stress disorder
Time frame: 34 days
Comparison of propranolol therapeutic effects versus placebo on symptom provocation state in traumatized subjects with and without posttraumatic stress disorder
Time frame: 34 days
Comparison of activated neuronal networks when a patient remember a pleasant , unpleasant or traumatic event
Time frame: 34 days
Comparison of emotional status of traumatized subjects with and without posttraumatic stress disorder
Time frame: 34 days
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A grip of 2 tablets of 20 mg each took 90 min before the emotional memory reactivation and the anatomical and functional exploration in fMRI