Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
327645 | Journal of Psychiatric Research | 2013 | 4 Pages |
Dopaminergic mechanisms may be involved in the pathophysiology of posttraumatic stress disorder (PTSD), although the evidence for this is limited; serotonergic mechanisms are implicated largely by virtue of the modest efficacy of serotonergic drugs in the treatment of the disorder. Basal cerebrospinal fluid (CSF) dopamine and serotonin metabolite concentrations are normal in PTSD patients. However, in the present experiment, we postulated that perturbations in CSF dopamine and serotonin metabolites could be induced by acute psychological stress. Ten volunteers with war-related chronic PTSD underwent 6-h continuous lumbar CSF withdrawal on two occasions per patient (6–9 weeks apart), using a randomized, within subject-controlled, crossover design. During one session a 1-h video with trauma-related footage (traumatic video) was shown and in the other session subjects viewed a 1-h neutral video. We quantified the dopamine metabolite homovanillic acid (HVA) and the serotonin metabolite 5-hydroxyindoleacetic acid (5-HIAA) in CSF at 10-min intervals, before, during, and after video provocation. Blood pressure, heart rate, and subjective anxiety and mood were monitored. Significant drop in mood and increases in anxiety and blood pressure occurred during the traumatic relative to the neutral movie. CSF HVA concentrations diminished significantly after the traumatic video (p < 0.05), in comparison with the neutral, while 5-HIAA tended to diminish (p < 0.10). We conclude that an acute decline in CNS HVA concentrations is associated with laboratory-induced symptoms in chronic PTSD patients. While further research is required to determine if the stress-induced dopaminergic changes are normative or pathological, the present data suggest that increasing dopaminergic neurotransmission be explored as a potential therapy, or adjunctive therapy, for PTSD.