Radio Electric Asymmetric Conveyer Neurobiological Treatments in Non-Specific Neck Pain: A Retrospective Study.

INTRODUCTION: Non-specific neck pain (NSNP) is a rather common symptomatology, and various therapeutic approaches are aimed to treat it, in the field of manual therapy, physiotherapy and pharmacology. METHODS: This retrospective study analyzes 65 subjects treated for NSNP with a neurobiological stimulation administered by medical devices based on radio electric asymmetric conveyer (REAC) technology. Initially, a neuro stimulation treatment called neuro postural optimization (NPO) was administered to improve the coordination of muscle activity and reduce adaptive decompensations. Subsequently, the bio stimulation treatment called tissue optimization (TO) was administered to reduce the algodystrophic and muscle contracture component. The evaluation of the efficacy of these treatments was made through the subjective evaluation of pain by the patients. Data were collected by the use of the numeric pain rating scale (NPRS) and neck pain questionnaire (NPQ), administered before the treatments and at the end of the cycle of therapy. RESULTS: The analysis of the results shows that this type of approach and treatment scheme is effective in reducing the symptoms of NSNP in both male and female subjects, regardless of their age. Other subjective data not quantified in this study but reported by all subjects, during and after the treatment cycle, were a feeling of lower stiffness of neck and shoulder, a reduction in the thickening of the cervicobrachial tissues, and a clear and progressive reduction of pain perception during the skin rolling (SR) maneuver. CONCLUSION: The combination of REAC-NPO neuromodulation and REAC-TO biomodulation treatments used in this study was shown to be effective in NPRS.

Alterations in the brain adenosine metabolism cause behavioral and neurological impairment in ADA-deficient mice and patients.

Adenosine Deaminase (ADA) deficiency is an autosomal recessive variant of severe combined immunodeficiency (SCID) caused by systemic accumulation of ADA substrates. Neurological and behavioral abnormalities observed in ADA-SCID patients surviving after stem cell transplantation or gene therapy represent an unresolved enigma in the field. We found significant neurological and cognitive alterations in untreated ADA-SCID patients as well as in two groups of patients after short- and long-term enzyme replacement therapy with PEG-ADA. These included motor dysfunction, EEG alterations, sensorineural hypoacusia, white matter and ventricular alterations in MRI as well as a low mental development index or IQ. Ada-deficient mice were significantly less active and showed anxiety-like behavior. Molecular and metabolic analyses showed that this phenotype coincides with metabolic alterations and aberrant adenosine receptor signaling. PEG-ADA treatment corrected metabolic adenosine-based alterations, but not cellular and signaling defects, indicating an intrinsic nature of the neurological and behavioral phenotype in ADA deficiency.