RESUMEN
Background Fluctuating asymmetry (FA) is widely defined as the deviation from perfect bilateral symmetry and is considered an epigenetic measure of environmental stress. Rinaldi and Fontani hypothesized that the FA morpho-functional changes originate from an adaptive motor behavior determined by functional alterations in the cerebellum and neural circuits, not caused by a lesion, but induced by environmental stress. They called this phenomenon functional dysmetria (FD). On this premise, they developed the radio electric asymmetric conveyer (REAC) technology, a neuromodulation technology aimed at optimizing the best neuro-psycho-motor strategies in relation to environmental interaction. Aims Previous studies showed that specific REAC neuro postural optimization (NPO) treatment can induce stable FD recovery. This study aimed to verify the duration of the NPO effect in inducing the stable FD recovery over time. Materials and methods Data were retrospectively collected from a population of 29,794 subjects who underwent a specific semiological FD assessment and received the NPO treatment, regardless of the pathology referred. Results The analysis of the data collected by the various participants in the study led us to ascertain the disappearance of FD in 100% of the cases treated, with a stability of the result detected up to 18 years after the single administration of the REAC NPO treatment. Conclusions The REAC NPO neurobiological modulation treatment consisting of a single administration surprisingly maintains a very long efficacy in the correction of FD. This effect can be explained as the long-lasting capacity of the NPO treatment to induce greater functional efficiency of the brain dynamics as proven in previous studies.
RESUMEN
OBJECTIVES: Severe traumatic brain injury (TBI) is associated with a 30-70% mortality rate. Nevertheless, controversy has been raised concerning the prognostic value of biomarkers following severe TBI. Therefore, our aim was to determine whether sFas or TNFalpha serum levels correlate with primary outcome following isolated severe TBI. METHODS: Seventeen consecutive male patients, victims of isolated severe TBI (Glasgow Coma Scale score 3-8) and a control group consisting of 6 healthy male volunteers were enrolled in this prospective study. Clinical outcome variables of severe TBI comprised: survival, time for intensive care unit (ICU) discharge, and neurological assessment by Glasgow Outcome Scale at ICU discharge. Venous blood samples were taken at admission in the ICU. Serum sFas and TNFalpha concentrations were measured by ELISA assays. RESULTS: At admission in the ICU (mean time 10.2 h after injury), mean sFas and TNFalpha concentrations were significantly increased in the TBI (0.105 and 24.275 rhog/l, respectively) compared with the control group (0.047 and 15.475 rhog/l, respectively). However, no significant correlation was found between higher serum sFas or TNFalpha concentrations and fatal outcome. CONCLUSIONS: Increased serum sFas and TNFalpha levels following isolated severe TBI did not predict fatal outcome.