RESUMEN
Brachial plexus trauma (BPT) often affects young patients and may result in lasting functional deficits. Standard care following BPT involves monitoring for clinical and electrophysiological evidence of muscle reinnervation, with surgical treatment decisions based on the presence or absence of spontaneous recovery. Data are emerging to suggest that central and peripheral adaptation may play a role in recovery following BPT. The present review highlights adaptive and maladaptive mechanisms of central and peripheral nervous system changes following BPT that may contribute to functional outcomes. Rehabilitation and other treatment strategies that harness or modulate these intrinsic adaptive mechanisms may improve functional outcomes following BPT.
Asunto(s)
Adaptación Fisiológica/fisiología , Brazo/inervación , Plexo Braquial/lesiones , Plexo Braquial/fisiopatología , Encéfalo/fisiopatología , Músculo Esquelético/inervación , Regeneración Nerviosa/fisiología , Adulto , Apraxias/fisiopatología , Traumatismos del Nacimiento/diagnóstico , Traumatismos del Nacimiento/fisiopatología , Traumatismos del Nacimiento/rehabilitación , Traumatismos del Nacimiento/cirugía , Plexo Braquial/cirugía , Neuropatías del Plexo Braquial/fisiopatología , Neuropatías del Plexo Braquial/cirugía , Terapia Combinada , Electromiografía , Femenino , Humanos , Lactante , Recién Nacido , Masculino , Embarazo , Estimulación Eléctrica Transcutánea del NervioRESUMEN
OBJECTIVE: Our goal is to develop a novel method to repair damaged axons. This method relies on acutely restoring axonal continuity rather than the traditional approach of promoting axonal regeneration. METHODS: Micro- and nanoechnological methods, in combination with focal application of electrical fields, are applied to individual and groups of axons both in vitro and in vivo. RESULTS: Application of these techniques has permitted micromanipulation of axons at the cellular level and fusion of axonal membranes. CONCLUSION: Although a great deal more work is necessary, our findings suggest that it may one day be possible to repair acutely disrupted axons by splicing their membranes back together.
Asunto(s)
Regeneración Nerviosa/fisiología , Procedimientos Neuroquirúrgicos/métodos , Nervios Periféricos/cirugía , Enfermedades del Sistema Nervioso Periférico/cirugía , Axones/fisiología , Axones/efectos de la radiación , Axones/ultraestructura , Membrana Celular/fisiología , Membrana Celular/ultraestructura , Terapia por Estimulación Eléctrica/métodos , Campos Electromagnéticos , Humanos , Microcirugia/métodos , Nanotecnología/métodos , Nanotecnología/tendencias , Regeneración Nerviosa/efectos de la radiación , Nervios Periféricos/patología , Nervios Periféricos/fisiopatología , Enfermedades del Sistema Nervioso Periférico/patología , Enfermedades del Sistema Nervioso Periférico/fisiopatología , Recuperación de la Función/fisiología , Recuperación de la Función/efectos de la radiaciónRESUMEN
Therapeutic options for amyotrophic lateral sclerosis (ALS), the most common adult-onset motor neuron disorder, remain limited. Emerging evidence from clinical studies and transgenic mouse models of ALS suggests that cannabinoids, the bioactive ingredients of marijuana (Cannabis sativa) might have some therapeutic benefit in this disease. However, Delta(9)-tetrahydrocannabinol (Delta(9)-THC), the predominant cannabinoid in marijuana, induces mind-altering effects and is partially addictive, compromising its clinical usefulness. We therefore tested whether cannabinol (CBN), a non-psychotropic cannabinoid, influences disease progression and survival in the SOD1 (G93A) mouse model of ALS. CBN was delivered via subcutaneously implanted osmotic mini-pumps (5 mg/kg/day) over a period of up to 12 weeks. We found that this treatment significantly delays disease onset by more than two weeks while survival was not affected. Further research is necessary to determine whether non-psychotropic cannabinoids might be useful in ameliorating symptoms in ALS.