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Puntos para una lectura rapida • Aunque es posible que en la lumbalgia mecanica se requiera fisioterapia, manipulacion y/o medicacion, el elemento central es el ejercicio. • El movimiento de inclinacion hacia delante forma parte de la gran mayoria de las acciones que se realizan a lo largo del dia. • En el movimiento de recuperacion de la postura erecta tras la inclinacion hacia delante, la region lumbar funciona como una palanca de 3.er grado. • La lumbalgia inespecifica se produce en estas dos situaciones que ocupan toda la vida: el mantenimiento de la postura y el movimiento. • El ejercicio es util en la lumbalgia cronica para reducir el dolor, aumentar la funcionalidad y acelerar la vuelta a las actividades normales diarias y al trabajo. • En el movimiento de todo el organismo actuan todos los musculos, bien de forma estatica o bien dinamica. • La practica de cualquier tipo de ejercicio aerobico puede servir para mantener una buena salud de la region lumbar en personas con posturas ortostaticas normales. • El metodo pilates es util en la lumbalgia cronica, pero en la misma medida que cualquier otro programa que se articule con ejercicios de la region lumbar. • A partir de las dos primeras semanas del comienzo de la lumbalgia, se puede iniciar un programa de ejercicios terapeuticos que trabajen la flexion, extension, flexion lateral y rotacion de la region lumbar. • En la hernia de disco se pueden hacer ejercicios isometricos de la musculatura abdominal porque no producen flexion de la region lumbar.

It is unclear how engaging in physical activity after long periods of inactivity provides expected health benefits.To determine whether physically inactive primary care patients reduce their mortality risk by increasing physical activity, even in low doses.Prospective cohort of 3357 physically inactive patients attending 11 Spanish public primary healthcare centres.Change in physical activity was repeatedly measured during patients' participation in the 'Experimental Program for Physical Activity Promotion' clinical trial between 2003 and 2006, using the '7-day Physical Activity Recall'. Mortality to 31 December 2018 (312 deaths) was recorded from national statistics, and survival time from the end of the clinical trial analysed using proportional hazard models.After 46 191 person-years of follow-up, compared with individuals who remained physically inactive, the mortality rates of those who achieved the minimum recommendations of 150-300 min/week of moderate- or 75-150 min/week of vigorous-intensity exercise was reduced by 45% (adjusted hazard ratio [aHR] 0.55; 95% confidence interval [95% CI] = 0.41 to 0.74); those who did not meet these recommendations but increased physical activity in low doses, that is, 50 min/week of moderate physical activity, showed a 31% reduced mortality (aHR 0.69, 95% CI = 0.51 to 0.93); and, those who surpassed the recommendation saw a 49% reduction in mortality (aHR 0.51, 95% CI = 0.32 to 0.81). The inverse association between increased physical activity and mortality follows a continuous curvilinear dose-response relationship.Physically inactive primary care patients reduced their risk of mortality by increasing physical activity, even in doses below recommended levels. Greater reduction was achieved through meeting physical activity recommendations or adopting levels of physical activity higher than those recommended.

Objective Corticospinal tract (CST) dysfunction is common in the pre-ataxic stage of spinocerebellar ataxia type 2 (SCA2) but quantitative assessment of its progression over time has not been explored. The aim of this study was to quantify the progression of CST dysfunction in pre-ataxic SCA2 using transcranial magnetic stimulation (TMS). Methods Thirty-three pre-ataxic SCA2 mutation carriers and a 33 age- and gender-matched healthy controls were tested at baseline and 2-years follow-up by standardized clinical exams, validated clinical scales, and TMS. Results Pre-ataxic SCA2 mutation carriers showed a significant increase of resting motor thresholds (RMT) to abductor pollicis brevis (APB) and tibialis anterior (TA) muscles, and of central motor conduction time (CMCT) to TA at 2-years follow-up, over and above changes in healthy controls. The changes in the pre-ataxic SCA2 mutation carriers were independent of the presence of clinical signs of CST dysfunction at baseline, and independent of conversion to clinically definite SCA2 at 2-years follow-up. Conclusions TMS markers of CST dysfunction progress significantly during the pre-ataxic stage of SCA2. Significance TMS measures of CST dysfunction may provide biomarkers of disease progression prior to clinical disease expression that have potential utility for monitoring neuroprotective therapies in future clinical trials.

Background Cognitive decline is a common non-motor feature characterizing Spinocerebellar Ataxia type 2 (SCA2) during the prodromal stage, nevertheless a reduced number of surrogate biomarkers of these alterations have been described. Objective To provide insights into cognitive dysfunction in SCA2 patients using P300 event-related potentials (ERP) and to evaluate these measures as biomarkers of the disease. Methods A cross-sectional study was performed with 30 SCA2 patients, 20 preclinical carriers and 33 healthy controls, who underwent visual, auditory P300 ERPs, and neurological examinations and ataxia scoring. Results SCA2 patients showed significant increase in P300 latencies and decrease of P300 amplitudes for visual and auditory stimuli, whereas preclinical carriers exhibit a less severe, but significant prolongation of P300 latencies. Multiple regression analyses disclosed a significant effect of SARA score on visual P300 abnormalities in patients as well as of the time to ataxia onset on visual P300 latencies in preclinical carriers. Conclusions This paper demonstrated the role of P300 ERP for the study of attentional, discriminative and working memory abnormalities in SCA2 patients and for the search of surrogate biomarkers from prodromal to the symptomatic stages. Moreover, our findings provide psychophysiological evidences supporting the cerebellar involvement in cognitive processes and allows us to identify promising outcome measures for future trials focusing on cognitive dysfunction.