Intermittent Hypoxia-Induced Enhancements in Corticospinal Excitability Predict Gains in Motor Learning and Metabolic Efficiency.

Acute intermittent hypoxia (AIH) enhances human motor function after incomplete spinal cord injury. Although the underlying mechanisms in humans are unknown, emerging evidence indicates that AIH facilitates corticospinal excitability to the upper limb. However, the functional relevance of this plasticity remains unexplored, and it is unclear whether similar plasticity can be induced for lower limb motor areas. We recently demonstrated that AIH improves motor learning and metabolic efficiency during split-belt walking. Thus, we hypothesized that AIH increases lower limb excitability and that these enhancements would predict the magnitude of motor learning and the corresponding reductions in net metabolic power. We assessed tibialis anterior (TA) excitability using transcranial magnetic stimulation and quantified changes in spatiotemporal asymmetries and net metabolic power in response to split-belt speed perturbations. We show that AIH enhances TA excitability, and that the magnitude of this facilitation positively correlates with greater spatiotemporal adaptation. Notably, we demonstrate a novel association between increased excitability and reduced net metabolic power during motor learning and savings. Together, our results suggest that AIH-induced gains in excitability predict both the magnitude of motor learning and the associated metabolic efficiency. Determining indices of AIH-induced improvements in motor performance is critical for optimizing its therapeutic reach.

Establishing a Comprehensive Wound Care Team and Program.

A comprehensive, interdisciplinary wound care team is of great importance to the management of acute, chronic, and recurrent wounds. This management functions best for the patient when all members of the team are in regular discussion regarding the wound care plan, providing more efficient and timelier patient-centered care. This article reviews the roles of different disciplines in the management of wounds. These disciplines include rehabilitation physicians, wound care nurses, registered nurses and certified nursing assistants, surgical teams, specialists of infectious diseases and mental health, dieticians, and patients and caregivers. A case study is also provided.

Emerging Technologies in the Wound Management Field.

Technological advances are incorporated into wound care management to enhance prevention through specialty mattresses and pressure mapping, assessment using modern imaging, and treatment with dressings and active therapies. We review specific equipment and evidence-based practice in the context of managing pressure injuries in patients with spinal cord injury.

Wheelchair Mobility-Related Injuries Due to Inadvertent Lower Extremity Displacement on Footplates: Analysis of the FDA MAUDE Database From 2014 to 2018.

OBJECTIVES: The aims of the study were to assess reports of wheelchair mobility-related injuries from inadvertent lower extremity displacement (ILED) on footplates, which were submitted to the Food and Drug Administration Manufacturer and User Facility Device Experience (MAUDE) database during 2014-2018, characterize injury types, and evaluate MAUDE data quality. METHODS: A systematic MAUDE database review was performed. Annual reports were searched using keywords: (a) "power wheelchair" and "injury" and (b) "mechanical (also known as manual) wheelchair" and "injury." Reports related to injuries from ILED on the footplate were reviewed. RESULTS: Reports of 1075 wheelchair injuries were found across the review period. Twenty nine (3%) met our inclusion criteria. The most common source of reports was "manufacturer." The wheelchair was unavailable for evaluation in 55.17% of reports. Manufacturers' submission dates (number of days that passed after they were notified) ranged from 3 to 159. Reported injuries decreased by 60% from 2014 to 2018. The end user used a power wheelchair for all but one report. The most common injuries were single fractures, multiple fractures, wounds/cuts/infections, and amputations (in order of incidence). The most common mechanism was the foot slipping off the footplate during wheelchair mobility. CONCLUSIONS: We observed inherent weaknesses in the MAUDE database reporting process and a concerning level of reporting bias. Although there were limited reports of injuries related to ILED on the footplate during wheelchair mobility, the injuries reported were significant. More standardized reporting of the mechanism and impact of these injuries is needed to better inform wheelchair design, prescription, and patient/family education.

Giving uridine and/or docosahexaenoic acid orally to rat dams during gestation and nursing increases synaptic elements in brains of weanling pups.

Developing neurons synthesize substantial quantities of membrane phospholipids in producing new synapses. We investigated the effects of maternal uridine (as uridine-5'-monophosphate) and docosahexaenoic acid supplementation on pups' brain phospholipids, synaptic proteins and dendritic spine densities. Dams consumed neither, 1 or both compounds for 10 days before parturition and 20 days while nursing. By day 21, brains of weanlings receiving both exhibited significant increases in membrane phosphatides, various pre- and postsynaptic proteins (synapsin-1, mGluR1, PSD-95), and in hippocampal dendritic spine densities. Administering these phosphatide precursors to lactating mothers or infants could be useful for treating developmental disorders characterized by deficient synapses.

Synaptic proteins and phospholipids are increased in gerbil brain by administering uridine plus docosahexaenoic acid orally.

The synthesis of brain phosphatidylcholine may utilize three circulating precursors: choline; a pyrimidine (e.g., uridine, converted via UTP to brain CTP); and a PUFA (e.g., docosahexaenoic acid); phosphatidylethanolamine may utilize two of these, a pyrimidine and a PUFA. We observe that consuming these precursors can substantially increase membrane phosphatide and synaptic protein levels in gerbil brains. (Pyrimidine metabolism in gerbils, but not rats, resembles that in humans.) Animals received, daily for 4 weeks, a diet containing choline chloride and UMP (a uridine source) and/or DHA by gavage. Brain phosphatidylcholine rose by 13-22% with uridine and choline alone, or DHA alone, or by 45% with the combination, phosphatidylethanolamine and the other phosphatides increasing by 39-74%. Smaller elevations occurred after 1-3 weeks. The combination also increased the vesicular protein Synapsin-1 by 41%, the postsynaptic protein PSD-95 by 38% and the neurite neurofibrillar proteins NF-70 and NF-M by up to 102% and 48%, respectively. However, it had no effect on the cytoskeletal protein beta-tubulin. Hence, the quantity of synaptic membrane probably increased. The precursors act by enhancing the substrate saturation of enzymes that initiate their incorporation into phosphatidylcholine and phosphatidylethanolamine and by UTP-mediated activation of P2Y receptors. Alzheimer's disease brains contain fewer and smaller synapses and reduced levels of synaptic proteins, membrane phosphatides, choline and DHA. The three phosphatide precursors might thus be useful in treating this disease.