Recovery from muscle weakness by exercise and FES: lessons from Masters, active or sedentary seniors and SCI patients.

Many factors contribute to the decline of skeletal muscle that occurs as we age. This is a reality that we may combat, but not prevent because it is written into our genome. The series of records from World Master Athletes reveals that skeletal muscle power begins to decline at the age of 30 years and continues, almost linearly, to zero at the age of 110 years. Here we discuss evidence that denervation contributes to the atrophy and slowness of aged muscle. We compared muscle from lifelong active seniors to that of sedentary elderly people and found that the sportsmen have more muscle bulk and slow fiber type groupings, providing evidence that physical activity maintains slow motoneurons which reinnervate muscle fibers. Further, accelerated muscle atrophy/degeneration occurs with irreversible Conus and Cauda Equina syndrome, a spinal cord injury in which the human leg muscles may be permanently disconnected from the nervous system with complete loss of muscle fibers within 5-8 years. We used histological morphometry and Muscle Color Computed Tomography to evaluate muscle from these peculiar persons and reveal that contraction produced by home-based Functional Electrical Stimulation (h-bFES) recovers muscle size and function which is reversed if h-bFES is discontinued. FES also reverses muscle atrophy in sedentary seniors and modulates mitochondria in horse muscles. All together these observations indicate that FES modifies muscle fibers by increasing contractions per day. Thus, FES should be considered in critical care units, rehabilitation centers and nursing facilities when patients are unable or reluctant to exercise.

Electroacupuncture improves voiding function in patients with neurogenic urinary retention secondary to cauda equina injury: results from a prospective observational study.

OBJECTIVE: To report the therapeutic effectiveness and feasibility of electroacupuncture (EA) treatment in patients with urinary retention which is caused by cauda equina injury and refractory to conventional conservative treatments. METHODS: From 9 August 2007 to 10 May 2010 prospective evaluation was carried out in 15 patients with neurogenic urinary retention secondary to cauda equina injury who underwent EA treatment at bilateral points BL32, BL33 and BL35. All patients received five sessions of EA treatment each week for the first 4 weeks, three sessions a week for the following 2 weeks, and then were followed up for 6 months. Voiding abilities, postvoiding residual urine volume (RUV) and maximum urinary flow rate (Qmax) were documented as outcome measures. RESULTS: After 6 weeks' EA treatment, 10/15 enrolled patients regained their self-voiding ability, and the mean postvoiding RUV for all patients decreased by 303.6±148.8 ml. In nine patients with documented data, Qmax increased by 11.0±6.3 ml/s. In nine patients, voiding difficulties changed from severe to mild. At the end of 6 months' follow-up, 8/10 patients retained their regained self-voiding ability, whereas two patients had lost their voiding ability again. CONCLUSION: The results indicate that the EA treatment may have longlasting therapeutic effectiveness in the management of neurogenic urinary retention secondary to cauda equina injury.

Strontium ranelate decreases the incidence of new caudal vertebral fractures in a growing mouse model with spontaneous fractures by improving bone microarchitecture.

UNLABELLED: Young mice over-expressing Runx2 fail to gain bone relative to wild type mice with growth and present spontaneous fractures. It allows, for the first time in rodents, direct assessment of anti-fracture efficacy of strontium ranelate which was able to decrease caudal vertebrae fracture incidence through an improvement of trabecular and cortical architecture. INTRODUCTION: The aim was to investigate whether strontium ranelate was able to decrease fracture incidence in mice over-expressing Runx2, model of severe developmental osteopenia associated with spontaneous vertebral fractures. METHODS: Transgenic mice and their wild type littermates were treated by oral route with strontium ranelate or vehicle for 9 weeks. Caudal fracture incidence was assessed by repeated X-rays, resistance to compressive loading by biochemical tests, and bone microarchitecture by histomorphometry. RESULTS: Transgenic mice receiving strontium ranelate had significantly fewer new fractures occurring during the 9 weeks of the study (-60%, p < 0.05). In lumbar vertebrae, strontium ranelate improves resistance to compressive loading (higher ultimate force to failure, +120%, p < 0.05) and trabecular microarchitecture (higher bone volume and trabecular number, lower trabecular separation, +60%, +50%, -39%, p < 0.05) as well as cortical thickness (+17%, p < 0.05). In tibiae, marrow cavity cross-section area and equivalent diameter were lower (-39%, -21%, p < 0.05). The strontium level in plasma and bone was in the same range as the values measured in treated postmenopausal women. CONCLUSIONS: This model allows, for the first time, direct assessment of anti-fracture efficacy of strontium ranelate treatment in rodents. In these transgenic mice, strontium ranelate was able to decrease caudal vertebral fracture incidence through an improvement of trabecular and cortical architecture.

Recovery of long-term denervated human muscles induced by electrical stimulation.

We investigated the restorative potential of intensive electrical stimulation in a patient with long-standing quadriceps denervation. Stimulation started 18 months after injury. After 26 months, the thighs were visibly less wasted. Muscle cross-sectional areas, measured by computerized tomography, increased from 36.0 cm(2) to 57.9 cm(2) (right) and from 36.1 cm(2) to 52.4 cm(2) (left). Knee torque had become sufficient to maintain standing without upper extremity support. Biopsies revealed evidence of both growth and regeneration of myofibers. The results suggest that electrical stimulation may offer a route to the future development of mobility aids in patients with lower motor neuron lesions.

Caudal spinal cord ischemia after lumbar vertebral manipulation.

Neurological complications after lumbar spine manipulation are uncommon. The cause is usually a herniated disk or displaced bony structure. We report a case of paraplegia that developed a few hours after manipulation of the lumbar spine. Magnetic resonance imaging was consistent with ischemia of the caudal spinal cord. No disk fragment or bony structure impinging on the spinal cord was seen. Spinal cord ischemia may deserve to be added to the list of possible adverse events after lumbar spine manipulation.

Vascular complication involving the conus medullaris or cauda equina after vertebral manipulation for an L4-L5 disk herniation.

A case of injury to the cauda equina or conus medullaris after lumbar vertebral manipulation is reported. In contrast to all other previously reported cases, no migrated disk fragment was demonstrated. Similar to experience at the cervical spine, lumbar vertebral manipulation may carry a risk of vascular injury. The neurological manifestations in our patient were consistent with compression of the Desproges-Gotteron artery by a small L4-L5 disk herniation.

Management of the neurogenic bowel in patients with spinal cord injury.

Bowel dysfunction in patients with spinal cord injury has a significant impact on quality of life as well as causing morbidity and death. This article reviews the pathophysiologic features of the neurogenic bowel of patients with spinal cord injury. Also discussed are the clinical manifestations, current options for management, and newer approaches that address this chronic and debilitating problem.

Cauda equina syndrome secondary to an improperly placed nucleotome probe.

Automated percutaneous lumbar discectomy has been shown to be a low morbidity procedure in the treatment of contained herniated lumbar discs. Described in this paper is a complication, i.e., a cauda equina syndrome secondary to a Nucleotome probe improperly placed in the thecal sac. The authors reemphasize the landmarks for the thecal sac, i.e., the medial border of the pedicles, and discuss the preventable nature of this type of complication.

Experimental evaluation of the urethral response to section of the spinal cord or cauda equina and to the electrostimulation of the bladder in non-human primates.

Studies of urethral function in 32 female monkeys indicate a dual innervation of the mid-urethra from sympathetic and somatic supply. The resting urethral pressure profiles were preserved after low level section of the spinal cord or division of the cauda equina. They had lowered amplitude after overstretch or electrostimulation of the autonomous bladder.