Context
Serotonergic dysfunction is implicated in the pathogenesis of posttraumatic stress disorder (PTSD), and recent animal models suggest that disturbances in serotonin type 1B receptor function, in particular, may contribute to chronic anxiety. However, the specific role of the serotonin type 1B receptor has not been studied in patients with PTSD.
Objective
To investigate in vivo serotonin type 1B receptor expression in individuals with PTSD, trauma-exposed control participants without PTSD (TC), and healthy (non–trauma-exposed) control participants (HC) using positron emission tomography and the recently developed serotonin type 1B receptor selective radiotracer [11C]P943.
Design
Cross-sectional positron emission tomography study under resting conditions.
Setting
Academic and Veterans Affairs medical centers.
Participants
Ninety-six individuals in 3 study groups: PTSD (n=49), TC (n=20), and HC (n=27).
Main Outcome Measure
Regional [11C]P943 binding potential (BPND) values in an a priori–defined limbic corticostriatal circuit investigated using multivariate analysis of variance and multiple regression analysis.
Results
A history of severe trauma exposure in the PTSD and TC groups was associated with marked reductions in [11C]P943 BPND in the caudate, the amygdala, and the anterior cingulate cortex. Participant age at first trauma exposure was strongly associated with low [11C]P943 BPND. Developmentally earlier trauma exposure also was associated with greater PTSD symptom severity and major depression comorbidity.
Conclusions
These data suggest an enduring effect of trauma history on brain function and the phenotype of PTSD. The association of early age at first trauma and more pronounced neurobiological and behavioral alterations in PTSD suggests a developmental component in the cause of PTSD.
Necrotizing fasciitis (NF) is a rapidly progressive soft tissue infection involving primarily the superficial fascia and subcutaneous tissue. The disease is caused by Streptococcus pyogenes or synergistic infection of anaerobic and facultative anaerobic bacteria. Further characteristics are severe, intolerable pain and a mortality rate of 30 to 50%. The NF can be initiated after surgical procedures, minor trauma, trivial scratches, in the setting of a chronic wound, or even in apparently intact skin. The age of the patient is not relevant for the prognosis of NF. As it is shown in this reported case, a young and previously healthy patient died after aesthetic liposuction in the course of a NF. Necrotizing fasciitis is a rare disease, therefore, it is important to review its diagnostic and clinical features, because only early diagnosis and prompt, radical surgery improves the survival rate.
Availability of nicotinic acetylcholine receptors containing beta2 subunits (beta2-nAChRs) was studied in unmedicated, symptomatic patients with post-traumatic stress disorder (PTSD) and healthy control subjects, all current non-smokers. A subgroup of participants had a history of smoking. Availability of beta2-nAChRs in the mesiotemporal cortex, prefrontal cortex, thalamus and striatum was determined using the radiotracer [123I]5-IA-85380 ([123I]5-IA) and single-photon emission computed tomography (SPECT). PTSD symptoms were assessed using the Clinician-Administered PTSD Scale (CAPS). Never-smoking PTSD patients compared to never-smoking healthy controls showed significantly higher [123I]5-IA binding in the mesiotemporal cortex (ANOVA: F=6.21, d.f.=1, 11, p=0.030). Among all PTSD patients, there was a significant correlation between the re-experiencing symptom cluster and thalamic [123I]5-IA binding (R2=0.66, p=0.019, Bonferroni corrected). These findings not only suggest an involvement of beta2-nAChRs in the pathophysiology of PTSD but also raise the possibility that this receptor may be a novel molecular target for drug development.
The results of the present study indicate a withdrawal-persisting dopaminergic imbalance in abstinent addicts as measured by a suggested peripheral marker.
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